Journal of internal medicine
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Multicenter Study
Do patient characteristics or factors at resuscitation influence long-term outcome in patients surviving to be discharged following in-hospital cardiac arrest?
Few studies have focused on factors influencing long-term outcome following in-hospital cardiac arrest. The present study assesses whether long-term outcome is influenced by difference in patient factors or factors at resuscitation. ⋯ Several patient factors, mainly age, functional status and co-morbid disease, influence long-term survival following cardiac arrest in hospital. The location where the arrest occurred also influences survival, but initial rhythm, delay to defibrillation and to return of spontaneous circulation do not.
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The association between HLA class II alleles and susceptibility to sarcoidosis is well documented. Further, the HLA-DRB1 15 and DQB1 0602 haplotype has been considered as a marker for both chronic and severe disease. Splenomegaly has been proposed as a marker for severity and activity in sarcoidosis, although its functional mechanism is unknown. In other diseases, HLA class II alleles can be markers for splenomegaly. We therefore set out to test the hypothesis that the primary DRB1 15-DQB1 0602 link in sarcoidosis would be to splenomegaly. ⋯ We conclude that in the Japanese population the primary association of HLA class II DQB1 0602 is with splenomegaly. This allele is also a marker for chronicity and lung disease severity. On the other hand, the presence of splenomegaly is a marker for severity and activity. Further studies are needed to explore the relationship between splenomegaly and sarcoidosis in other ethnic groups and its association with HLA-DQB1 0602.
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Obesity induces an inflammation state that is implicated in many clinically important complications, including insulin resistance, diabetes, atherosclerosis and non-alcoholic fatty liver disease. Although the cause and the molecular participants in this process remain incompletely defined, adipose tissue has a central role. ⋯ More recently a critical role for immune cells, specifically mononuclear phagocytes, in generating the obesity-induced inflammation has been identified. Defining the molecular and cellular components of obesity-induced inflammation offers the potential of identifying therapeutic targets that can ameliorate the complications associated with obesity.