Is age a limiting factor for adaptation to cochlear implant?

The influence of age on adaptation to cochlear implant (CI) is still being contested in the literature. The aim of this study was twofold. First, hearing outcomes in quiet conditions were compared between CI users implanted over and under the age of 70 years. Second, the effect of the duration of auditory deprivation was investigated. The study design is a retrospective review and the setting is in academic tertiary referral center. One hundred and twenty-one postlingually deafened implanted adults participated in this study. Hearing outcomes were compared between 121 postlingually deafened adults implanted under 40, between 40 and 70, and over 70 years of age. Speech audiometry measurements were taken at 1, 3, 6, 12, 24 and 60 months post-cochlear implantation (pCI), in quiet conditions only. Hearing outcomes were significantly better only at 1 year pCI in the youngest group compared to the two older groups. No significant difference was observed between the middle-aged and eldest subjects at any time. The influence of the severe-to-profound hearing loss (SPHL) duration was investigated and found to be equally distributed among the different age groups. Good hearing outcomes in elderly patients are not secondary to a difference in SPHL duration. Age should not be a limiting factor for cochlear implantation decision.

Intracardiac allogeneic mesenchymal stem cell transplantation elicits neo-angiogenesis in a fully immunocompetent ischaemic swine model.

OBJECTIVES: Autologous mesenchymal stem cell transplantation has been shown to improve myocardial function in ischaemic cardiomyopathy. We studied one hypothetical mechanism, neo-angiogenesis, using allogeneic mesenchymal stem cell transplantation in an ischaemic swine model. METHODS: Allogeneic mesenchymal stem cells were injected in the peri-infarct area (1×10(6) cells kg(-1)) 2 weeks after myocardial infarction. Myocardial infarction alone (n=3) served as a control group. In the myocardial infarction-mesenchymal stem cells group (n=6), tacrolimus was given from day 0 to day 12. Capillary density and inflammatory/rejection processes (anti-factor VIII and anti-CD3/CD68 monoclonal antibodies, respectively) were compared between groups. RESULTS: In scarred myocardium, capillary density was similar between both ischaemic groups: 15.4 (±15.3) and 14.7 (±15.2) vessel/field in myocardial infarction-mesenchymal stem cells and myocardial infarction-alone groups (non-significant). In viable myocardium adjacent to the infarction, capillary density was significantly increased in the myocardial infarction-mesenchymal stem cells group than in the myocardial infarction-alone group (p=0.002). The number of infiltrating CD3+ cells was equivalent in both myocardial infarction-alone and myocardial infarction-mesenchymal stem cells groups (CD3+: 8.6% vs 9.3%, non-significant). However, CD68+ cell infiltration was more prominent after mesenchymal stem cell transplantation (4.7% vs 2% in myocardial infarction alone, p<0.01). CONCLUSIONS: Allogeneic mesenchymal stem cell transplantation enhances angiogenesis after myocardial infarction. This effect is limited to the viable myocardium. Using a concomitant 12-day course of tacrolimus, no mesenchymal stem cell-specific cellular immune response was demonstrated.

Prenatal diagnosis of fetal cataract: case report and review of the literature.

OBJECTIVES: To report a case of prenatally diagnosed fetal cataract and conduct a systematic review of previously reported cases. METHODS: Review of the literature based mainly on Pubmed search using specific keywords in order to list cataract causes diagnosed prenatally and in early childhood, isolated or associated with microphthalmia. RESULTS AND DISCUSSION: A differential diagnosis list and specific prenatal diagnosis testing are suggested in order to offer the best management of this rare fetal condition.

Inhibition of humoral response to allogeneic porcine mesenchymal stem cell with 12 days of tacrolimus.

BACKGROUND: In vivo studies have highlighted allogeneic mesenchymal stem-cell (MSC) immunogenicity. We investigated in vitro MSC-immunosuppressive drugs interaction and further tested in vivo the humoral response to intracardiac allogeneic MSC transplantation in a mini-swine model receiving a short course of immunosuppression. METHODS: For in vitro experiments, long-term culture MSCs were used. Immunosuppressive drugs tested were mycophenolate mofetil, cyclosporin, tacrolimus (TAC), sirolimus (SIR), and everolimus. Cell proliferation/viability was assessed on day 7. For each drug, the C50 was determined, and the agonistic effect between immunosuppressive drugs and MSCs on alloreactivity was measured in proliferation assay of MSC-peripheral blood mononuclear cell cultures. For in vivo experiments, one-haplotype swine leukocyte antigen class I and II mismatch (n=11) were used. Allogeneic MSCs were transplanted into ischemic myocardium. TAC was administered 12 days. Donor-specific antibody response was assessed by flow cytometry and complement-mediated cytotoxicity assay. RESULTS: All drugs except TAC significantly decreased cell proliferation (from 17% to 62%). In MSC-peripheral blood mononuclear cell co-culture assay, MSCs' immunomodulatory properties were maintained when TAC or SIR were used. In vivo experiments showed that only 2 of 11 animals under TAC developed donor-specific antibodies. Importantly, sera from those two animals did not elicit a complement-mediated cytotoxic response. CONCLUSIONS: Immunosuppressive drugs significantly affect proliferation and viability of MSCs, but neither TAC nor SIR had a detrimental impact on MSCs' immunomodulatory properties. In this large-animal model, addition of short course of immunosuppression seems to overcome the immune response to intracardiac allogeneic MSCs, which was recently demonstrated to occur in the absence of immunosuppression.