Control of methicillin-resistant Staphylococcus aureus outbreak involving several hospitals.

This population-based, retrospective, cohort study describes a large methicillin-resistant Staphylococcus aureus (MRSA) epidemic caused by one strain (E1) in the greater Helsinki region. The epidemic comprised 210 cases at several hospitals, but was finally controlled. The study period ranged from June 1991 to December 2000.

ss-cell autoantibodies, human leukocyte antigen II alleles, and type 1 diabetes in autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy.

Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) is caused by lack of functional products of the autoimmune regulator gene located on chromosome 21q22.3. The patients are at high risk of developing insulin-dependent (type 1) diabetes, but the positive predictive value of GAD65 or islet cell antibodies for type 1 diabetes is only 27%.

Decreased expression of protectin (CD59) in gut epithelium in ulcerative colitis and Crohn's disease.

Without adequate protection, the cells of the human body would be susceptible to destruction by the complement system. The main defense against complement lysis is a molecule called protectin (CD59) that is widely distributed in human tissues. Because the complement system has been suggested to be involved in the pathogenesis of inflammatory bowel diseases, we examined the expression of protectin in the colonic epithelium of patients with ulcerative colitis or Crohn's disease and controls.

Antiphospholipid antibodies in children.

Sera from children (n = 173) were tested for antiphospholipid antibodies (aPL) using an enzyme immunoassay detecting IgG anti-cardiolipin antibodies (GPL). Sera from adults (n = 100) were also tested. GPL were detected more frequently and at higher levels in children than in adults.