Using Speech Recognition Software to Increase Writing Fluency for Individuals with Physical Disabilities

Writing is an important skill that is necessary throughout school and life. Many students with physical disabilities, however, have difficulty with writing skills due to disability-specific factors, such as motor coordination problems. Due to the difficulties these individuals have with writing, assistive technology is often utilized. One piece of assistive technology, speech recognition software, may help remove the motor demand of writing and help students become more fluent writers. Past research on the use of speech recognition software, however, reveals little information regarding its impact on individuals with physical disabilities. Therefore, this study involved students of high school age with physical disabilities that affected hand use. Using an alternating treatments design to compare the use of word processing with the use of speech recognition software, this study analyzed first-draft writing samples in the areas of fluency, accuracy, type of word errors, recall of intended meaning, and length. Data on fluency, calculated in words correct per minute (wcpm) indicated that all participants wrote much faster with speech recognition compared to word processing. However, accuracy, calculated as percent correct, was much lower when participants used speech recognition compared to word processing. Word errors and recall of intended meaning were coded based on type and varied across participants. In terms of length, all participants wrote longer drafts when using speech recognition software, primarily because their fluency was higher, and they were able, therefore, to write more words. Although the results of this study indicated that participants wrote more fluently with speech recognition, because their accuracy was low, it is difficult to determine whether or not speech recognition is a viable solution for all individuals with physical disabilities. Therefore, additional research is needed that takes into consideration the editing and error correction time when using speech recognition software

Loss of the alpha-isoform of calcineurin is sufficient to induce nephrotoxicity and altered expression of transforming growth factor-beta

BACKGROUND. Use of calcineurin inhibitors is frequently limited by fibrosis, closely linked with increased transforming growth factor (TGF)-ß. However, mechanisms of extracellular matrix expansion and TGFß regulation following calcineurin inhibition are unknown. Mice lacking specific calcineurin catalytic subunit isoforms may offer important insight into this pathway. METHODS. We compared mice lacking the α or ß isoform to a model of cyclosporin nephrotoxicity. Histological features common with cyclosporin nephrotoxicity including matrix expansion, arteriole hyalinization, and inflammation were assessed. Next, regulation specifically of fibronectin and TGFß was examined in vivo and in vitro. Finally, the role of TGFß in upregulation of fibronectin with loss of calcineurin activity was examined. RESULTS. Loss of the α isoform results in histologic features and matrix expansion similar to cyclosporin, whereas loss of the ß does not. Fibronectin and TGFß are increased and renal function is impaired in α-null and aged α+/-. In primary α-/- renal fibroblasts, nuclear translocation of the calcineurin substrate NFATc is normal but regulation is lost in ß-null fibroblasts, confirming that the isoforms have distinct functions. Consistent with in vivo findings, α-null cells have increased fibronectin and TGFß. However, neutralizing TGFß antibody did not reduce fibronectin accumulation. CONCLUSIONS. Our data show that calcineurin-α is key to regulation of fibrosis and TGFß and loss of this isoform reproduces features of cyclosporine nephrotoxicity in vivo and in vitro. In addition, we show that upregulation of TGFß and fibronectin likely result from a shared mechanism, but changes in fibronectin expression are independent of TGFß in renal fibroblasts. © 2007 Lippincott Williams & Wilkins, Inc

T-Cell Receptor-Stimulated Calcineurin Activity Is Inhibited in Isolated T Cells from Transplant Patients

The addition of calcineurin inhibitors, including cyclosporine A (CsA) and FK-506 (tacrolimus), to transplant protocols has markedly reduced acute allograft rejection and prolonged patient survival. Although monitoring of serum drug levels has been shown to be a poor indicator of efficacy, there is little data on calcineurin enzymatic activity in humans. Therefore, we measured calcineurin in isolated CD3+/4+ T cells from 81 non-transplant controls and 39 renal allograft patients by using a 32PO4-labeled calcineurin-specific substrate. A gender difference was observed in the control cohort, with activity in males significantly higher than that in females (1073 ± 134 versus 758 ± 75 fmol/μg/min, respectively). Activity of both groups was comparably inhibited by 5 ng/ml tacrolimus (27 ± 4 versus 30 ± 4%). Calcineurin is a downstream target of the T-cell receptor (TCR). Therefore, activity was measured in isolated T cells after incubation with anti-CD3/CD28 antibodies to stimulate the TCR. Calcineurin activity increased significantly from 1214 ± 111 to 1652 ± 138 fmol/μg/min; addition of either tacrolimus or CsA (500 ng/ml) blocked CD3/CD28 stimulation. Despite therapeutic levels of tacrolimus and CsA (mean 11.4 and 172 ng/ml), basal calcineurin activity was significantly higher among renal transplant recipients than controls (1776 ± 175 versus 914 ± 78 fmol/μg/min). In contrast, anti-CD3/CD28 antibodies failed to stimulate calcineurin activity in transplant subjects. Finally, we found that basal and stimulated calcineurin activities are inversely related. Consistent with this finding, basal activity in resting T cells rose over time after transplant but stimulation fell (r2 = 0.785, p < 0.05). These data suggest that examination of TCR-stimulated calcineurin activity after renal transplantation may be useful for monitoring immunosuppression of individual patients