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ARTÍCULOS DE INTERÉS. ABSTRACT Y ENLACES



Chocolate consumption and risk of stroke

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A prospective cohort of men and meta-analysis

  1. Susanna C. Larsson, PhD,
  2. Jarmo Virtamo, MD and
  3. Alicja Wolk, DMSc
+ Author Affiliations
  1. From the Division of Nutritional Epidemiology (S.C.L., A.W.), Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden; and Department of Chronic Disease Prevention (J.V.), National Institute for Health and Welfare, Helsinki, Finland.
  2. Correspondence & reprint requests to Dr. Larsson: susanna.larsson@ki.se

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Abstract

Objective: To investigate the association between chocolate consumption and risk of stroke in men and conduct a meta-analysis to summarize available evidence from prospective studies of chocolate consumption and stroke.
Methods: We prospectively followed 37,103 men in the Cohort of Swedish Men. Chocolate consumption was assessed at baseline using a food-frequency questionnaire. Cases of first stroke were ascertained from the Swedish Hospital Discharge Registry. For the meta-analysis, pertinent studies were identified by searching the PubMed and EMBASE databases through January 13, 2012. Study-specific results were combined using a random-effects model.
Results: During 10.2 years of follow-up, we ascertained 1,995 incident stroke cases, including 1,511 cerebral infarctions, 321 hemorrhagic strokes, and 163 unspecified strokes. High chocolate consumption was associated with a lower risk of stroke. The multivariable relative risk of stroke comparing the highest quartile of chocolate consumption (median 62.9 g/week) with the lowest quartile (median 0 g/week) was 0.83 (95 % CI 0.70–0.99). The association did not differ by stroke subtypes. In a meta-analysis of 5 studies, with a total of 4,260 stroke cases, the overall relative risk of stroke for the highest vs lowest category of chocolate consumption was 0.81 (95% CI 0.73–0.90), without heterogeneity among studies (p = 0.47).
Conclusion: These findings suggest that moderate chocolate consumption may lower the risk of stroke.


Therapeutic Efficacy of CXCR3 Blockade in an Experimental Model of Severe Sepsis

Daniela S Herzig, Yin Guo, Geping Fang, Tracy E Toliver-Kinsky and Edward R Sherwood
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Critical Care 2012, 16:R168 doi:10.1186/cc11642
Published: 19 September 2012

Abstract (provisional)

In our previous studies, we demonstrated that CXCR3 participates in the regulation of lymphocyte trafficking during cecal ligation and puncture (CLP)-induced sepsis. In this study, we evaluated the effects of treatment with anti-CXCR3 IgG and antibiotics on outcome during septic shock caused by CLP. C57BL/6J mice were treated with neutralizing IgG against CXCR3 plus Primaxin at either 24 hours prior to or at 2 or 6 hours after CLP. Control mice received non-specific IgG plus Primaxin in the same regimen. Survival, core body temperature, bacterial clearance and systemic cytokine production were evaluated. Our results show that treatment with anti-CXCR3 IgG plus Primaxin significantly improved survival when administered at 24 hours prior to CLP (50 vs 10%), 2 hours after CLP (55 vs 10%) or 6 hours after CLP (55 vs 25%) compared to mice receiving non-specific IgG plus Primaxin. Treatment with anti-CXCR3 plus Primaxin at 24 hours prior to CLP attenuated hypothermia and IL-6 and MIP-2 production but did not alter bacterial clearance. Treatment with anti-CXCR3 IgG and Primaxin at 2 hours after CLP did not improve bacterial clearance and systemic cytokine production compared to mice treated with IgG and Primaxin, whereas at 6 hours after CLP, bacterial clearance and IL-6 and MIP-2 concentrations, both in plasma and peritoneal lavage fluid, were significantly improved in mice receiving anti-CXCR3 IgG and Primaxin compared to mice which only received non-specific IgG and Primaxin. The results from this study indicate that neutralization of CXCR3 prior to, 2 hours or 6 hours after the initiation of CLP-induced septic shock improves survival and attenuates CLP-induced inflammation and physiologic dysfunction.

La migraña como factor de riesgo vascular


Revisión

[REV NEUROL 2012;55:349-358] PMID: 22972577 - Revisión - Fecha de publicación: 16/09/2012
D. Larrosa-Campo, C.R. Carbajo, M. Para-Prieto, S. Calleja-Puerta, E. Cernuda-Morollón, J. Pascual

Introducción. Migraña e ictus se asocian con una frecuencia superior a lo esperable. Aunque controvertida, múltiples estudios demuestran una asociación significativa entre migraña y patología vascular no sólo cerebral, sino también en otros lechos arteriales. El espectro de la relación entre migraña e ictus comprende relaciones de coexistencia, semejanza y causalidad. Los mecanismos por los que la migraña llega a ser un factor de riesgo vascular y conduce al desarrollo de un ictus no son del todo conocidos, posiblemente porque sean múltiples, complejos e interrelacionados entre sí. Objetivo. Poniendo énfasis en los artículos más recientes, se revisa críticamente el estado actual acerca de la relación de causalidad entre migraña y enfermedad vascular, y se discute su fisiopatología. Desarrollo. La migraña es un factor de riesgo independiente de ictus, especialmente en el subgrupo de población comprendido por mujeres jóvenes, con migraña con aura, crisis frecuentes, fumadoras y en tratamiento con anticonceptivos orales. Además, se asocia con lesiones de la sustancia blanca y patología vascular en otros territorios arteriales. Disfunción del endotelio y musculatura vascular, hipercoagulabilidad, depresión propagada cortical, factores genéticos, foramen oval permeable, perfil desfavorable de riesgo vascular, disección arterial y el tratamiento específico de migraña se postulan como mecanismos patogénicos. Conclusiones. Si la enfermedad cerebrovascular es una importante causa de invalidez y mortalidad, y la migraña es un factor de riesgo de enfermedad vascular, comprender la relación entre migraña y enfermedad vascular es necesario para reducir riesgos y optimizar su manejo y tratamiento.