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In 16 mature New Zealand white rabbits mesenchymal stem cells were aspirated from the bone marrow, cultured in monolayer and implanted on to a full-thickness osteochondral defect artificially made on the patellar groove of the same rabbit. A further 13 rabbits served as a control group. The rabbits were killed after 14 weeks. Healing of the defect was investigated histologically using haematoxylin and eosin and Safranin-O staining and with immunohistochemical staining for type-II collagen. We also used a reverse transcription-polymerase chain reaction (RT-PCR) to detect mRNA of type-I and type-II collagen. The semiquantitative histological scores were significantly higher in the experimental group than in the control group (p < 0.05). In the experimental group immunohistochemical staining on newly formed cartilage was more intense for type-II collagen in the matrix and RT-PCR from regenerated cartilage detected mRNA for type-II collagen in mature chondrocytes. These findings suggest that repair of cartilage defects can be enhanced by the implantation of cultured mesenchymal stem cells.

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Background and Purpose: Patients with acute cardioembolic stroke frequently show hemorrhagic transformation (HTr). We attempted to identify predictors of symptomatic HTr in acute ischemic stroke with atrial fibrillation (AF). Methods: Of the consecutive acute ischemic stroke patients with AF at 12 hospitals in Korea, patients with posterior circulation stroke or thrombolytic therapy were excluded. Immediate anticoagulation was recommended to all patients, except those with: (1) large infarcts, 50% or more of the middle cerebral artery territory, (2) significant HTr on initial imaging, or (3) other safety concerns. Symptomatic HTr was defined as cerebral hemorrhage temporally related to neurological deterioration. Results: Of the 389 included patients (mean age 71 years), 260 (67%) were treated with anticoagulation within 1 week from the onset. Symptomatic HTr occurred in 4.6%. Large infarct (OR 6.38, 95% CI 1.16–35.14), previous hemorrhagic stroke (OR 10.67, 1.77–64.25), and low platelet count (OR per 10⁴ increase 0.87, 0.79–0.97) were independent predictors of symptomatic HTr. hsCRP values tended to be higher in patients with symptomatic HTr (p = 0.055). Conclusions: Caution is needed in anticoagulation treatment of acute cardioembolic stroke patients with a large infarct, previous hemorrhagic stroke, low platelet count, or a high hsCRP level.

In a large case-control study of Swedish incident type I diabetes patients and controls, 0-34 years of age, we tested the hypothesis that the GIMAP5 gene, a key genetic factor for lymphopenia in spontaneous BioBreeding rat diabetes, is associated with type I diabetes; with islet autoantibodies in incident type I diabetes patients or with age at clinical onset in incident type I diabetes patients. Initial scans of allelic association were followed by more detailed logistic regression modeling that adjusted for known type I diabetes risk factors and potential confounding variables. The single nucleotide polymorphism (SNP) rs6598, located in a polyadenylation signal of GIMAP5, was associated with the presence of significant levels of IA-2 autoantibodies in the type I diabetes patients. Patients with the minor allele A of rs6598 had an increased prevalence of IA-2 autoantibody levels compared to patients without the minor allele (OR=2.2; Bonferroni-corrected P=0.003), after adjusting for age at clinical onset (P=8.0 x 10(-13)) and the numbers of HLA-DQ A1*0501-B1*0201 haplotypes (P=2.4 x 10(-5)) and DQ A1*0301-B1*0302 haplotypes (P=0.002). GIMAP5 polymorphism was not associated with type I diabetes or with GAD65 or insulin autoantibodies, ICA, or age at clinical onset in patients. These data suggest that the GIMAP5 gene is associated with islet autoimmunity in type I diabetes and add to recent findings implicating the same SNP in another autoimmune disease.