Allogeneic hematopoietic stem cell transplantation (HSCT) is rarely performed in adult patients with sickle cell disease (SCD). We utilized the chemotherapy-free, alemtuzumab/total body irradiation 300 cGy regimen with sirolimus as post-transplantation immunosuppression in 13 high-risk SCD adult patients between November 2011 and June 2014. Patients received matched related donor (MRD) granulocyte colony-stimulating factor-mobilized peripheral blood stem cells, including 2 cases that were ABO incompatible. Quality-of-life (QoL) measurements were performed at different time points after HSCT. All 13 patients initially engrafted. A stable mixed donor/recipient chimerism was maintained in 12 patients (92%), whereas 1 patient not compliant with sirolimus experienced secondary graft failure. With a median follow-up of 22 months (range, 12 to 44 months) there was no mortality, no acute or chronic graft-versus-host disease (GVHD), and no grades 3 or 4 extramedullary toxicities. At 1 year after transplantation, patients with stable donor chimerism have normalized hemoglobin concentrations and improved cardiopulmonary and QoL parameters including bodily pain, general health, and vitality. In 4 patients, sirolimus was stopped without rejection or SCD-related complications. These results underscore the successful use of a chemotherapy-free regimen in MRD HSCT for high-risk adult SCD patients and demonstrates a high cure rate, absence of GVHD or mortality, and improvement in QoL including the applicability of this regimen in ABO mismatched cases (NCT number 01499888).

This very limited case series suggest there may be a role for therapeutic plasma exchange as a rescue therapy in severe shock and acute lung injury related to pH1N1 that has not responded to traditional therapy.

Body magnetic resonance (MR) imaging is challenging because of the complex interaction of multiple factors, including motion arising from respiration and bowel peristalsis, susceptibility effects secondary to bowel gas, and the need to cover a large field of view. The combination of these factors makes body MR imaging more prone to artifacts, compared with imaging of other anatomic regions. Understanding the basic MR physics underlying artifacts is crucial to recognizing the trade-offs involved in mitigating artifacts and improving image quality. Artifacts can be classified into three main groups: (a) artifacts related to magnetic field imperfections, including the static magnetic field, the radiofrequency (RF) field, and gradient fields; (b) artifacts related to motion; and (c) artifacts arising from methods used to sample the MR signal. Static magnetic field homogeneity is essential for many MR techniques, such as fat saturation and balanced steady-state free precession. Susceptibility effects become more pronounced at higher field strengths and can be ameliorated by using spin-echo sequences when possible, increasing the receiver bandwidth, and aligning the phase-encoding gradient with the strongest susceptibility gradients, among other strategies. Nonuniformities in the RF transmit field, including dielectric effects, can be minimized by applying dielectric pads or imaging at lower field strength. Motion artifacts can be overcome through respiratory synchronization, alternative k-space sampling schemes, and parallel imaging. Aliasing and truncation artifacts derive from limitations in digital sampling of the MR signal and can be rectified by adjusting the sampling parameters. Understanding the causes of artifacts and their possible solutions will enable practitioners of body MR imaging to meet the challenges of novel pulse sequence design, parallel imaging, and increasing field strength. © RSNA, 2015 • radiographics.rsna.org Susie Y. Huang, MD, PhD Ravi T. Seethamraju, PhD Pritesh Patel, MD Peter F. Hahn, MD, PhD John E. Kirsch, PhD Alexander R. Guimaraes, MD, PhD Abbreviations: B 0 = static magnetic field, B 1 = applied radiofrequency field, FOV = field of view, RARE = rapid acquisition with relaxation enhancement, RF = radiofrequency, SNR = signal-to-noise ratio, SSFP = steady-state free precession, STIR = short inversion time inversionrecovery, TR = repetition time

Amyloid-β (Aβ) peptide aggregation is known to play a central role in the etiology of Alzheimer’s disease (AD). Among various aggregates, low-molecular weight soluble oligomers of Aβ are increasingly believed to be the primary neurotoxic agents responsible for memory impairment. Anionic interfaces are known to influence the Aβ aggregation process significantly. Here, we report the effects of interfaces formed by medium-chain (C9–C12), saturated non-esterified fatty acids (NEFAs) on Aβ42 aggregation. NEFAs uniquely affected Aβ42 aggregation rates that depended on both the ratio of Aβ:NEFA as well the critical micelle concentration (CMC) of the NEFAs. More importantly, irrespective of the kind of NEFA used, we observed that two distinct oligomers, 12–18 mers and 4–5 mers were formed via different pathway of aggregation under specific experimental conditions: (i) 12–18 mers were generated near the CMC in which NEFAs augment the rate of Aβ42 aggregation towards fibril formation, and, (ii) 4–5 mers were formed above the CMC, where NEFAs inhibit fibril formation. The data indicated that both 12–18 mers and 4–5 mers are formed along an alternate pathway called ‘off-pathway’ that did not result in fibril formation and yet have subtle structural and morphological differences that distinguish their bulk molecular behavior. These observations, (i) reflect the possible mechanism of Aβ aggregation in physiological lipid-rich environments, and (ii) reiterate the fact that all oligomeric forms of Aβ need not be obligatory intermediates of the fibril formation pathway.