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        Gender Differences in Osteoporosis: A Single-Center Observational Study

        De Martinis Massimo,Sirufo Maria Maddalena,Polsinelli Matteo,Placidi Giuseppe,Di Silvestre Daniela,Ginaldi Lia 대한남성과학회 2021 The World Journal of Men's Health Vol.39 No.4

        Purpose: Osteoporosis affects more than 200 million people worldwide: its prevalence increases with age and is actually growing due to the constant population aging. Women are at greater risk than men, but in recent years it has become increasingly evident that osteoporosis represents a significantly important problem also for men. However, osteoporosis in men is still poorly studied, underdiagnosed and inadequately treated. Materials and Methods: We conducted an observational study to identify any gender disparities in osteoporosis screening. For this purpose we observed people consecutively admitted at our Outpatient Service for the Diagnosis of Osteoporosis during the last 3 years. Patients underwent clinical and laboratory assessment and bone mineral density (BMD) measurements by dual-energy X-ray absorptiometry. Bone turnover serum markers have been evaluated and stratified according to gender. Results: Out of 3,752 patients, 2,376 subjects who met the inclusion criteria were identified. As expected, the great majority (94.5%) of the screened subjects were women and only 5.4% were men. Women exhibited lower BMD compared to men (Tscore values: -2.33±1.14 vs. -1.31±1.55; p<0.001), whereas the prevalence of fractures in osteoporotic men was significantly higher (50% vs. 31%; p<0.001). Women had lower vitamin D and higher bone remodeling markers compared to men. Secondary osteoporosis was more frequent in men (66.67%) than in women (20.83%) and the calculated risk for hip fractures was higher in osteoporotic men compared to women (11.47±10.62 vs. 6.87±7.73; p<0.001). Conclusions: Here we highlighted that men are under-screened for osteoporosis and exhibit secondary osteoporosis more frequently than women.

      • KCI등재

        The role of pulmonary ORCC and CLC-2 channels in the response to oxidative stress

        Canella Rita,Benedusi Mascia,Martini Marta,Guiotto Anna,Cervellati Franco,Valacchi Giuseppe 대한독성 유전단백체 학회 2021 Molecular & cellular toxicology Vol.17 No.3

        Background Exposure of human lung epithelial cells to the oxidant pollutant ozone (O3) alters cell Cl− currents inducing an outward rectifier effect. Among the various Cl− channels, ClC-2 and ORCC seemed to be involved in this response. Objectives To identify the channel related to O3 induced current changes. Results Down regulating the expression of ORCC and ClC-2 genes and analyzing the membrane current show that the enhancement of the current disappeared when ORCC was silenced. The contribution of ORCC and ClC-2 channels in control and O3 treated cells was obtained by a mathematical approach. Conclusion We suggest that O3 activates ORCC channels and slightly inhibited ClC-2 channels in the negative voltage range. These findings open the possibility of identifying the biomolecular changes induced by O3 allowing a possible pharmacological intervention towards chloride current due to oxidative stress. Background Exposure of human lung epithelial cells to the oxidant pollutant ozone (O3) alters cell Cl− currents inducing an outward rectifier effect. Among the various Cl− channels, ClC-2 and ORCC seemed to be involved in this response. Objectives To identify the channel related to O3 induced current changes. Results Down regulating the expression of ORCC and ClC-2 genes and analyzing the membrane current show that the enhancement of the current disappeared when ORCC was silenced. The contribution of ORCC and ClC-2 channels in control and O3 treated cells was obtained by a mathematical approach. Conclusion We suggest that O3 activates ORCC channels and slightly inhibited ClC-2 channels in the negative voltage range. These findings open the possibility of identifying the biomolecular changes induced by O3 allowing a possible pharmacological intervention towards chloride current due to oxidative stress.

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        Arterial Stiffness in Patients with Deep and Lobar Intracerebral Hemorrhage

        Maurizio Acampa,Francesca Guideri,Ilaria Di Donato,Rossana Tassi,Giovanna Marotta,Giuseppe Lo Giudice,Paolo D’Andrea,Giuseppe Martini 대한뇌졸중학회 2014 Journal of stroke Vol.16 No.3

        Background and Purpose Intracerebral hemorrhage (ICH) accounts for approximately 10% of stroke cases. Hypertension may play a role in the pathogenesis of ICH that occurs in the basal ganglia, thalamus, pons, and cerebellum, but not in that of lobar ICH. Hypertension contributes to decreased elasticity of arteries, thereby increasing the likelihood of rupture in response to acute elevation in intravascular pressure. This study aimed to evaluate arterial stiffness (using the arterial stiffness index [ASI]) in patients with deep (putaminal and thalamic) ICH in comparison with patients with lobar ICH. Methods We enrolled 64 patients (mean±SD age: 69.3±10.7 years; 47 men and 17 women) among 73 who referred consecutively to our department for intraparenchymal hemorrhage and underwent brain computed tomography (CT) and cerebral angio-CT. In all the subjects, 24-hour heart rates and blood pressures were monitored. The linear regression slope of diastolic on systolic blood pressure was assumed as a global measure of arterial compliance, and its complement (1 minus the slope), ASI, has been considered as a measure of arterial stiffness. Results In the patients with deep ICH, ASI was significantly higher than in the patients with lobar ICH (0.64±0.19 vs. 0.53±0.17, P=0.04). Conclusions Our results suggest that in deep ICH, arterial stiffening represents a possible pathogenetic factor that modifies arterial wall properties and contributes to vascular rupture in response to intravascular pressure acute elevation. Therapeutic strategies that reduce arterial stiffness may potentially lower the incidence of deep hemorrhagic stroke.

      • KCI등재

        Ischemic Stroke after Heart Transplantation

        Maurizio Acampa,Pietro Enea Lazzerini,Francesca Guideri,Rossana Tassi,Giuseppe Martini 대한뇌졸중학회 2016 Journal of stroke Vol.18 No.2

        Cerebrovascular complications after orthotopic heart transplantation (OHT) are more common in comparison with neurological sequelae subsequent to routine cardiac surgery. Ischemic stroke and transient ischemic attack (TIA) are more common (with an incidence of up to 13%) than intracranial hemorrhage (2.5%). Clinically, ischemic stroke is manifested by the appearance of focal neurologic deficits, although sometimes a stroke may be silent or manifests itself by the appearance of encephalopathy, reflecting a diffuse brain disorder. Ischemic stroke subtypes distribution in perioperative and postoperative period after OHT is very different from classical distribution, with different pathogenic mechanisms. Infact, ischemic stroke may be caused by less common and unusual mechanisms, linked to surgical procedures and to postoperative inflammation, peculiar to this group of patients. However, many strokes (40%) occur without a well-defined etiology (cryptogenic strokes). A silent atrial fibrillation (AF) may play a role in pathogenesis of these strokes and P wave dispersion may represent a predictor of AF. In OHT patients, P wave dispersion correlates with homocysteine plasma levels and hyperhomocysteinemia could play a role in the pathogenesis of these strokes with multiple mechanisms increasing the risk of AF. In conclusion, stroke after heart transplantation represents a complication with considerable impact not only on mortality but also on subsequent poor functional outcome.

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