Masthead,Volume 65, Issue 1

At sufficiently high Larmor frequencies, traveling electromagnetic waves along a magnet bore can be used for remote magnetic resonance excitation and detection, effectively using the bore as a waveguide. So far, this approach has relied only on the lowest waveguide modes and thus has not supported multiple‐channel operation for radiofrequency shimming and parallel imaging. In this work, this limitation is addressed by establishing a larger number of propagating modes and tapping their spatial field diversity with multiple waveguide ports. The number of available modes is increased by loading with dielectric inserts; the ports are implemented by stub and loop couplers at the end of a waveguide extension. The resulting traveling‐wave array, operated at 298 MHz in a 7T whole‐body magnet, is shown to enable radiofrequency shimming as well as parallel imaging with commonly used acceleration factors. The last part of the study concerns the amount of dielectric loading that is required. For the given Larmor frequency and bore dimensions, it is found that rather few water‐filled inserts, occupying ～5% of the bore cross‐section, are sufficient for effective parallel imaging. Magn Reson Med, 2011. © 2011 Wiley‐Liss, Inc.     

Valvular Heart Disease: Assessment of Valve Morphology and Quantification Using MR

For clinical evaluation and decision-making in patients with valvular heart disease, the diagnostic armamentarium expands steadily. This evolution makes it difficult to choose the most appropriate approach for a specific valvular lesion. It may also reflect our uncertainty of what are the findings that best predict clinical outcome of patients, e.g. after surgery. Accordingly, for each type of valvular lesion, some pathopysiological considerations are stated in order to derive the most important measures that would allow optimal guidance of patients. Based on these considerations the value of an MR study is discussed for each valvular lesion. Newest advances in MR technology allow for highly accurate measurements of regurgitant volumes and hence, MR may be the method of choice for a quantitative evaluation of regurgitant valves. For assessment of stenosis severity, measurement of transvalvular pressure gradient is an appropriate measure and MR may not confer benefits over echocardiography, provided the ultrasound window is adequate (and stroke volume is in the normal range). With respect to surgical treatment, valvular morphology is of pivotal importance, particularly for the mitral valve, and echocardiography still appears to be the first line method. Little data relate lesion severity and/or morphology to clinical outcome. Conversely, the extent of cardiac adaptation to pressure- and/or volume-overload, i.e. ventricular remodeling, is a strong predictor of outcome, and is therefore most important for final judgement of the patient. For assessment of left and right ventricular remodeling, echocardiography typically provides all the necessary information. However, in special cases with discrepant findings, with inadequate ultrasound window, or in the preoperative work-up, MR may provide important information regarding cardiac adaptation to valvular lesion.     

Protective effect of parvalbumin on excitotoxic motor neuron death

The mechanism responsible for the selective vulnerability of motor neurons in amyotrophic lateral sclerosis (ALS) is poorly understood. Several lines of evidence indicate that susceptibility of motor neurons to Ca(2+) overload induced by excitotoxic stimuli is involved. In this study, we investigated whether the high density of Ca(2+)-permeable AMPA receptors on motor neurons gives rise to higher Ca(2+) transients in motor neurons compared to dorsal horn neurons. Dorsal horn neurons were chosen as controls as these cells do not degenerate in ALS. In cultured spinal motor neurons, the rise of the cytosolic Ca(2+) concentration induced by kainic acid (KA) and mediated by the AMPA receptor was almost twice as high as in spinal neurons from the dorsal horn. Furthermore, we investigated whether increasing the motor neuron's cytosolic Ca(2+)-buffering capacity protects them from excitotoxic death. To obtain motor neurons with increased Ca(2+) buffering capacity, we generated transgenic mice overexpressing parvalbumin (PV). These mice have no apparent phenotype. PV overexpression was present in the central nervous system, kidney, thymus, and spleen. Motor neurons from these transgenic mice expressed PV in culture and were partially protected from KA-induced death as compared to those isolated from nontransgenic littermates. PV overexpression also attenuated KA-induced Ca(2+) transients, but not those induced by depolarization. We conclude that the high density of Ca(2+)-permeable AMPA receptors on the motor neuron's surface results in high Ca(2+) transients upon stimulation and that the low cytosolic Ca(2+)-buffering capacity of motor neurons may contribute to the selective vulnerability of these cells in ALS. Overexpression of a high-affinity Ca(2+) buffer such as PV protects the motor neuron from excitotoxicity and this protective effect depends upon the mode of Ca(2+) entry into the cell.     

Is impingement the cause of jumper's knee? Dynamic and static magnetic resonance imaging of patellar tendinitis in an open-configuration system

BACKGROUND: Chronic overload is considered the main cause of patellar tendinitis, but it has been postulated that impingement of the inferior patellar pole against the patellar tendon during knee flexion could be responsible. HYPOTHESIS: The role of the patellar pole in patellar tendinitis can be determined by dynamic magnetic resonance imaging. STUDY DESIGN: Case-control study. METHODS: We compared 19 knees with patellar tendinitis and 32 asymptomatic knees of age-matched subjects using an open-configuration magnetic resonance imaging system. Dynamic sagittal images were obtained from full extension to 100 degrees of flexion with and without activation of the quadriceps muscle. The following measurements were made from the images: tendon-patella angle, anteroposterior diameter of the tendon, signal difference-to-noise ratio, the shape of the inferior patellar pole, and the location of the patellar tendon insertion. RESULTS: The tendon-patella angle was not significantly different between groups at any flexion angle, with or without quadriceps muscle activation. The insertion site of the patellar tendon differed significantly but not the shape of the inferior pole of the patella. The volume and the signal difference-to-noise ratio of zones of increased intratendinous signal as well as the anteroposterior diameter of the proximal patellar tendon were increased in symptomatic knees. CONCLUSIONS: The relationship between the patella and the patellar tendon was identical in both groups; therefore, chronic overload seems to be a major cause of patellar tendinitis.     

Interleukin-8 expression by fetal and neonatal pulmonary cells in hyaline membrane disease and amniotic infection

IL-8, a chemokine with striking neutrophil-activating properties, is important in the pathogenesis of various disorders of the adult lung. Little is known about its production and possible role in fetal and neonatal lung disorders. We therefore examined IL-8 expression by immunohistochemistry in lung tissue from neonates with hyaline membrane disease, from fetuses with amniotic infection, and from a fetal control group with noninflammatory diseases. In the majority of cases with hyaline membrane disease, intense IL-8 immunoreaction was seen in fetal and neonatal neutrophils and in almost half of these cases, in epithelial cells of the terminal airways as well as in the connective tissue cell compartment. In contrast, in the amniotic infection group, strong IL-8 immunostaining was almost exclusively seen in maternal aspirated neutrophils. Little or no IL-8 signal was seen in the control cases in all cell types examined. Also, no IL-8 production by fetal lung cells was detected in fetuses <18 wk of gestation. The marked presence of IL-8 in all cell types of the lung in hyaline membrane disease cases indicates a role for IL-8 in the pathobiology of hyaline membrane disease possibly similar to that in adult respiratory distress syndrome. It further suggests that the cytokine network of the fetal lung is already well developed by the second trimester of pregnancy.     

MALT1 and the API2-MALT1 fusion act between CD40 and IKK and confer NF-kappa B-dependent proliferative advantage and resistance against FAS-induced cell death in B cells

The most frequently recurring translocations in mucosa-associated lymphoid tissue (MALT) B-cell non-Hodgkin lymphoma, t(11;18)(q21;q21) and t(14;18)(q32; q21), lead to formation of an API2-MALT1 fusion or IgH-mediated MALT1 overexpression. Various approaches have implicated these proteins in nuclear factor kappaB (NF-kappa B) signaling, but this has not been shown experimentally in human B cells. Immunohistochemistry showed that MALT1 is predominantly expressed in normal and malignant germinal center B cells, corresponding to the differentiation stage of MALT lymphoma. We expressed MALT1 and apoptosis inhibitor-2 API2/MALT1 in human B-cell lymphoma BJAB cells and found both transgenes in membrane lipid rafts along with endogenous MALT1 and 2 binding partners involved in NF-kappa B signaling, B-cell lymphoma 10 (BCL10) and CARMA1 (caspase recruitment domain [CARD]-containing membrane-associated guanylate kinase [MAGUK] 1). API2-MALT1 and exogenous MALT1 increased constitutive NF-kappa B activity and enhanced I kappa B kinase (IKK) activation induced by CD40 stimulation. Both transgenes protected BJAB cells from FAS (CD95)-induced death, consistent with increases in NF-kappa B cytoprotective target gene expression, and increased their proliferation rate. Expression of a dominant-negative I kappa B alpha mutant showed that these survival and proliferative advantages are dependent on elevated constitutive NF-kappa B activity. Our findings support a model in which NF-kappa B signaling, once activated in a CD40-dependent immune response, is maintained and enhanced through deregulation of MALT1 or formation of an API2-MALT1 fusion.