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Current Approaches to the Treatment of Post-Stroke Aphasia
Julius Fridriksson,Argye Elizabeth Hillis 대한뇌졸중학회 2021 Journal of stroke Vol.23 No.2
Aphasia, impairment of language after stroke or other neurological insult, is a common and often devastating condition that affects nearly every social activity and interaction. Behavioral speech and language therapy is the mainstay of treatment, although other interventions have been introduced to augment the effects of the behavioral therapy. In this narrative review, we discuss advances in aphasia therapy in the last 5 years and focus primarily on properly powered, randomized, controlled trials of both behavioral therapies and interventions to augment therapy for post-stroke aphasia. These trials include evaluation of behavioral therapies and computer-delivered language therapies. We also discuss outcome prediction trials as well as interventional trials that have employed noninvasive brain stimulation, or medications to augment language therapy. Supported by evidence from Phase III trials and large meta-analyses, it is now generally accepted that aphasia therapy can improve language processing for many patients. Not all patients respond similarly to aphasia therapy with the most severe patients being the least likely responders. Nevertheless, it is imperative that all patients, regardless of severity, receive aphasia management focused on direct therapy of language deficits, counseling, or both. Emerging evidence from Phase II trials suggests transcranial brain stimulation is a promising method to boost aphasia therapy outcomes.
Fault reactivation potential during $CO_2$ injection in the Gippsland Basin, Australia
Ruth, Peter J. van,Nelson, Emma J.,Hillis, Richard R. Korean Society of Earth and Exploration Geophysici 2006 지구물리와 물리탐사 Vol.9 No.1
The risk of fault reactivation in the Gippsland Basin was calculated using the FAST (Fault Analysis Seal Technology) technique, which determines fault reactivation risk by estimating the increase in pore pressure required to cause reactivation within the present-day stress field. The stress regime in the Gippsland Basin is on the boundary between strike-slip and reverse faulting: maximum horizontal stress $({\sim}\;40.5\;Mpa/km)$ > vertical stress (21 Mpa/km) ${\sim}$ minimum horizontal stress (20 MPa/km). Pore pressure is hydrostatic above the Campanian Volcanics of the Golden Beach Subgroup. The NW-SE maximum horizontal stress orientation $(139^{\circ}N)$ determined herein is broadly consistent with previous estimates, and verifies a NW-SE maximum horizontal stress orientation in the Gippsland Basin. Fault reactivation risk in the Gippsland Basin was calculated using two fault strength scenarios; cohesionless faults $(C=0;{\mu}=0.65)$ and healed faults $(C=5.4;\;{\mu}=0.78)$. The orientations of faults with relatively high and relatively low reactivation potential are almost identical for healed and cohesionless fault strength scenarios. High-angle faults striking NE-SW are unlikely to reactivate in the current stress regime. High-angle faults oriented SSE-NNW and ENE-WSW have the highest fault reactivation risk. Additionally, low-angle faults (thrust faults) striking NE-SW have a relatively high risk of reactivation. The highest reactivation risk for optimally oriented faults corresponds to an estimated pore pressure increase (Delta-P) of 3.8 MPa $({\sim}548\;psi)$ for cohesionless faults and 15.6 MPa $({\sim}2262\;psi)$ for healed faults. The absolute values of pore pressure increase obtained from fault reactivation analysis presented in this paper are subject to large errors because of uncertainties in the geomechanical model (in situ stress and rock strength data). In particular, the maximum horizontal stress magnitude and fault strength data are poorly constrained. Therefore, fault reactivation analysis cannot be used to directly measure the maximum allowable pore pressure increase within a reservoir. We argue that fault reactivation analysis of this type can only be used for assessing the relative risk of fault reactivation and not to determine the maximum allowable pore pressure increase a fault can withstand prior to reactivation.
Quintero, Jesus,Juamperez, Javier,Gonzales, Emmanuel,Julio, Ecaterina,Mercadal-Hally, Maria,Collado-Hilly, Mauricette,Marin-Sanchez, Ana,Charco, Ramon The Korean Society of Pediatric Gastroenterology 2020 Pediatric gastroenterology, hepatology & nutrition Vol.23 No.2
We present an 8 years old girl who was diagnosed at 6 months of age of Progressive Familial Intrahepatic Cholestasis type 2. Although liver transplantation (LT) was classically considered curative for these patients, cholestasis recurrence with normal gamma-glutamyl transpeptidase (GGT), mediated by anti-bile salt export pump (BSEP) antibodies after LT (auto-antibody Induced BSEP Deficiency, AIBD) has been recently reported. Our patient underwent LT at 14 months. During her evolution, patient presented three episodes of acute rejection. Seven years after the LT, the patient presented pruritus with cholestasis and elevation of liver enzymes with persistent normal GGT. Liver biopsy showed intrahepatic cholestasis and giant-cell transformation with very low BSEP activity. Auto-antibodies against BSEP were detected therefore an AIBD was diagnosed. She was treated with Rituximab and immunoadsorption with resolution of the AIBD. As a complication of the treatment she developed a pneumocystis infection successfully treated with corticoids, cotrimoxazol and anidulafungin.
Jesús Quintero,Javier Juamperez,Emmanuel Gonzales,Ecaterina Julio,Maria Mercadal-Hally,Mauricette Collado-Hilly,Ana Marín-Sánchez,Ramon Charco 대한소아소화기영양학회 2020 Pediatric gastroenterology, hepatology & nutrition Vol.23 No.2
We present an 8 years old girl who was diagnosed at 6 months of age of Progressive Familial Intrahepatic Cholestasis type 2. Although liver transplantation (LT) was classically considered curative for these patients, cholestasis recurrence with normal gamma-glutamyl transpeptidase (GGT), mediated by anti-bile salt export pump (BSEP) antibodies after LT (auto-antibody Induced BSEP Deficiency, AIBD) has been recently reported. Our patient underwent LT at 14 months. During her evolution, patient presented three episodes of acute rejection. Seven years after the LT, the patient presented pruritus with cholestasis and elevation of liver enzymes with persistent normal GGT. Liver biopsy showed intrahepatic cholestasis and giant-cell transformation with very low BSEP activity. Auto-antibodies against BSEP were detected therefore an AIBD was diagnosed. She was treated with Rituximab and immunoadsorption with resolution of the AIBD. As a complication of the treatment she developed a pneumocystis infection successfully treated with corticoids, cotrimoxazol and anidulafungin.