Xueqian Deng

Objectives: The aim of the current study was to differentiate between neural activity that represents neural anomalies that are responsible for persistent developmental stuttering from the activity that is a result of compensating for stuttering. This was done by investigating alterations to the intrinsic functional architecture of speech-language processes of patients with PDS before and after a short-term intervention. Methods: The resting-state functional connectivity and cortical thickness were examined before and after the intervention. The structural data were used to validate the functional results. Fifteen stuttering patients who received intervention, 13 stuttering patients who did not receive intervention, and 13 fluent controls participated. Results: Before the intervention, both groups of PDS patients showed significant RSFC and cortical thickness reductions in the left pars-opercularis and RSFC increases in the cerebellum, as compared to fluent controls. The intervention was effective in reducing stuttering in PDS- patients and lowering their RSFC in the cerebellum to the level of fluent controls. The intervention effect was specific to the PDS-group. The intervention did not change RSFC and cortical thickness in the left PO, which remained at its preintervention level. Conclusions: The results suggest that the left PO is a locus where the intrinsic functional architecture of speech-language processes is altered in PDS patients, suggesting an etiologic role of this region in PDS. The cerebellum showed intervention-induced neural reorganization, suggesting a compensatory response when stuttering occurs. Copyright © 2012 by AAN Enterprises, Inc.

© 2015 The Authors. Background: The significance of detection of Trypanosoma cruzi DNA in blood of antibody-positive patients for risk of development of Chagas heart disease is not well established. The objective of this study was to compare detection of T. cruzi DNA with known clinical and laboratory markers of Chagas cardiomyopathy severity. Methods: This is a case-control study nested within a retrospective cohort developed in Brazil to understand the natural history of Chagas disease. The study enrolled 499 T. cruzi seropositive blood donors and 488 frequency matched seronegative control donors who had donated between 1996 and 2002, and 101 patients with clinically diagnosed CC. In 2008-2010 all enrolled subjects underwent a health questionnaire, medical examination, electrocardiograms and echocardiograms and polymerase chain reaction analyses. A blinded panel of three cardiologists adjudicated the outcome of CC. Trypanosoma cruzi kinetoplast minicircle sequences were amplified by real-time PCR using an assay with a sensitivity of one parasite per 20mL of blood. All testing was performed on coded samples. Results: Rates of PCR detection of T. cruzi DNA were significantly higher in CC patients and SP-BD diagnosed with CC compared with SP-BD without CC. The presence of parasitaemia was significantly associated with known markers of disease progression such as QRS and QT interval duration, lower left ventricular ejection fraction, higher left ventricular index mass, and elevated troponin and NTpro-BNP levels. Conclusion: Trypanosoma cruzi PCR positivity is associated with presence and severity of cardiomyopathy, suggesting a direct role of parasite persistence in disease pathogenesis.