Gender health and policies: the state of the art from exposure to solutions

Objective. To synthesize the determinants of gender inequalities through a narrative review that: (i) describes gender related var- iables that can create different levels of health; (ii) describes key points that may assist in policy development and its reorientation towards gender differences; (iii) debates potential approaches in understanding gender issues. Methods. Review of the international literature through online databases (Pubmed), search engines, publications and documents from ?grey literature?. Inclusion criteria: publications from 1997, English language; keywords used: gender based analysis; gender and public policy; women?s health; gender differences; health policy; gender impact assessment. Among the 300 papers retrieved, 55 were selected for relevance. Results. We performed a narrative synthesis of the included literature, regarding: (i) gender differences and their determi-nants; (ii) elements for the changing; (iii) possible approaches; (iv) gender influences the pursuit of health and health care access through specific variables; (v) health policies can modify these variables only by a minimal percentage. These interventions should guarantee equity and allow efficient resources allocation. The gap between political announce- ments and real policy implementation remains unchanged. (vi) Standard approaches to the topic are not feasible due to the scarcity of a specific literature and the numerous cultural differences. Conclusions. Gender analysis of policies suggests they can dif- ferently affect women in comparison to men. However, reforms, strategies and interventions introduced in the last two decades, have achieved a limited success towards better gender equality in health. The main aim is to attack the structural sources of gender inequity in the society

Polymorphism of the Fractalkine Receptor CX3CR1 and Systemic Sclerosis-associated Pulmonary Arterial Hypertension

Fractalkine (FKN) and its receptor CX3CR1 are critical mediators in the vascular and tissue damage of several chronic diseases, including systemic sclerosis (SSc) and pulmonary arterial hypertension (PAH). Interestingly, the V249I and T280M genetic polymorphisms influence CX3CR1 expression and function. We investigated whether these polymorphisms are associated with PAH secondary to SSc. CX3CR1 genotypes were analyzed by PCR and sequencing in 76 patients with limited SSc and 204 healthy controls. PAH was defined by colorDoppler echocardiography. Homozygosity for 249II as well as the combined presence of 249II and 280MM were significantly more frequent in patients with SSc compared to controls (17 vs 6%, p = 0.0034 and 5 vs 1%, p = 0.0027, respectively). The 249I and 280M alleles were associated with PAH (odd ratio [OR] 2.2, 95% confidence interval [CI] 1.01-4.75, p = 0.028 and OR 7.37, 95%CI: 2.45-24.60, p = 0.0001, respectively). In conclusion, the increased frequencies of 249I and 280M CX3CR1 alleles in a subgroup of patients with SSc-associated PAH suggest a role for the fractalkine system in the pathogenesis of this condition. Further, the 249I allele might be associated with susceptibility to SSc

Polymorphism in the fractalkine receptor CX3CR1 as a genetic risk factor for coronary artery disease.

Abstract Fractalkine (FKN) and its receptor CX3CR1 are critical mediators in the vascular and tissue damage of several chronic diseases, including systemic sclerosis (SSc) and pulmonary arterial hypertension (PAH). Interestingly, the V249I and T280M genetic polymorphisms influence CX3CR1 expression and function. We investigated whether these polymorphisms are associated with PAH secondary to SSc. CX3CR1 genotypes were analyzed by PCR and sequencing in 76 patients with limited SSc and 204 healthy controls. PAH was defined by colorDoppler echocardiography. Homozygosity for 249II as well as the combined presence of 249II and 280MM were significantly more frequent in patients with SSc compared to controls (17 vs 6%, p ¼ 0.0034 and 5 vs 1%, p ¼ 0.0027, respectively). The 249I and 280M alleles were associated with PAH (odd ratio [OR] 2.2, 95% confidence interval [CI] 1.01 -4.75, p ¼ 0.028 and OR 7.37, 95%CI: 2.45 -24.60, p ¼ 0.0001, respectively). In conclusion, the increased frequencies of 249I and 280M CX3CR1 alleles in a subgroup of patients with SSc-associated PAH suggest a role for the fractalkine system in the pathogenesis of this condition. Further, the 249I allele might be associated with susceptibility to SSc