Impact of Gender on In-hospital Mortality in Patients with Acute Myocardial Infarction in Nagasaki

Acute myocardial infarction (AMI) is one of the leading causes of death in Japan. Immediate reperfusion therapy, includingcoronary intervention, improves patient prognosis. Despite this, females are said to be more prone to poor prognosis. A regional AMI registry in Nagasaki prefecture has been instituted recently that will evaluate whether female gender might predict short-term in-hospital death. Seventeen regional AMI centers enrolled all AMI patients from September 2014 through March 2016. A propensity score (PS) was derived using logistic regression to model the probability of females as a total function of the potential confounding covariates. Two types of PS techniques were used: PS matching and PS stratification. The consistency of in-hospital death was determined between PS matched patients of both genders. Based on PS, patients were ranked and stratified into five groups for the PS stratification. Out of 996 patients, 67 (6.7%) died during hospitalization: 31 (10.4%) out of 298 females and 36 (5.2%) out of 698 males (p < 0.0025). The proportion of cardiac and non-cardiac related death was almost same between genders (25 and 6 in female, 29 and 7 in male, respectively). Among 196 PS matched patients, there was a consistency between genders regarding in-hospital deaths (McNemar test, p = 0.6698). The 717 propensity scored patients had no significant differences between genders among propensity quintiles (Cochran-Mantel-Heanszel test, p = 0.7117). We found that gender alone is not an indicator of short-term in-hospital death in acute myocardial infarction patients

Impact of Gender on In-hospital Mortality in Patients with Acute Myocardial Infarction in Nagasaki

Acute myocardial infarction (AMI) is one of the leading causes of death in Japan. Immediate reperfusion therapy, including coronary intervention, improves patient prognosis. Despite this, females are said to be more prone to poor prognosis. A regional AMI registry in Nagasaki prefecture has been instituted recently that will evaluate whether female gender might predict short-term in-hospital death. Seventeen regional AMI centers enrolled all AMI patients from September 2014 through March 2016. A propensity score (PS) was derived using logistic regression to model the probability of females as a total function of the potential confounding covariates. Two types of PS techniques were used: PS matching and PS stratification. The consistency of in-hospital death was determined between PS matched patients of both genders. Based on PS, patients were ranked and stratified into five groups for the PS stratification. Out of 996 patients, 67 (6.7%) died during hospitalization: 31 (10.4%) out of 298 females and 36 (5.2%) out of 698 males (p < 0.0025). The proportion of cardiac and non-cardiac related death was almost same between genders (25 and 6 in female, 29 and 7 in male, respectively). Among 196 PS matched patients, there was a consistency between genders regarding in-hospital deaths (McNemar test, p = 0.6698). The 717 propensity scored patients had no significant differences between genders among propensity quintiles (Cochran-Mantel-Heanszel test, p = 0.7117). We found that gender alone is not an indicator of short-term in-hospital death in acute myocardial infarction patients

Follistatin improves skeletal muscle healing after injury and disease through an interaction with muscle regeneration, angiogenesis, and fibrosis

Recovery from skeletal muscle injury is often incomplete because of the formation of fibrosis and inadequate myofiber regeneration; therefore, injured muscle could benefit significantly from therapies that both stimulate muscle regeneration and inhibit fibrosis. To this end, we focused on blocking myostatin, a member of the transforming growth factorβ superfamily and a negative regulator of muscle regeneration, with the myostatin antagonist follistatin. In vivo, follistatin-overexpressing transgenic mice underwent significantly greater myofiber regeneration and had less fibrosis formation compared with wild-type mice after skeletal muscle injury. Follistatin's mode of action is likely due to its ability to block myostatin and enhance neovacularization. Furthermore, muscle progenitor cells isolated from follistatin-overexpressing mice were significantly superior to muscle progenitors isolated from wild-type mice at regenerating dystrophin-positive myofibers when transplanted into the skeletal muscle of dystrophic mdx/severe combined immunodeficiency mice. In vitro, follistatin stimulated myoblasts to express MyoD, Myf5, and myogenin, which are myogenic transcription factors that promote myogenic differentiation. Moreover, follistatin's ability to enhance muscle differentiation is at least partially due to its ability to block myostatin, activin A, and transforming growth factorβ1, all of which are negative regulators of muscle cell differentiation. The findings of this study suggest that follistatin is a promising agent for improving skeletal muscle healing after injury and muscle diseases, such as the muscular dystrophies. © 2011 American Society for Investigative Pathology

A Toolbox for Triticeae Genomics

International audienceIn the last two decades, progress in cereal genomics has been remarkable, enabling a better understanding of the structure and function of the cereal genomes. However, significant advances mainly concerned rice and maize, whereas for the Triticeae species, namely wheat, barley and rye, the development of genomic tools and resources has long been hampered by the size and the complexity of their genomes. Recently, new technologies have allowed the development of a toolbox for Triticeae genomics comparable to what is available for rice and maize. Triticeae scientists and breeders can now benefit from a wide range of tools, including molecular markers, genetic maps, EST sequences, microrarrays, BAC libraries and transformation systems that can be applied to structural, functional, evolutionary and comparative genomic studies of the Triticeae genomes