CT of the hip prosthesis: appearance of components, fixation, and complications.

Multidetector computed tomography (CT) is an excellent way to supplement the radiographic evaluation of problematic hip prostheses. Multidetector CT is well suited for assessing periprosthetic bone, determining precise acetabular cup position, and evaluating periprosthetic fluid collections or ossified masses. Metal implants pose a number of challenges in the performance and interpretation of CT examinations. However, metal artifacts can be minimized by decreasing the detector collimation and pitch, increasing the kilovolt peak and milliampere-seconds, and using appropriate reconstruction algorithms and section thickness. Image interpretation requires a basic understanding of hip reconstruction and hip implants, as well as use of a systematic method of analysis that incorporates prior radiographic findings and CT findings. Radiologists must be familiar with the normal and abnormal CT appearances of hip prostheses and be able to recognize common complications on CT scans.

Glenohumeral Joint Instability: A Review of Anatomy, Clinical Presentation, and Imaging.

The glenohumeral joint is intrinsically predisposed to instability because of the bony anatomy but maintained in alignment by many important structures, including the glenoid labrum, glenohumeral ligaments (GHLs), and muscles and tendons. Trauma and overuse can damage these stabilizers, which may then lead to subluxation or dislocation and eventually recurrent instability. This is most common in the anterior direction, which has several recognizable patterns of injury on advanced imaging, including humeral Hill Sachs deformities, bony Bankart lesion of the anteroinferior glenoid, soft tissue Bankart lesions, Bankart variant lesions (Perthes and ALPSA lesions), and HAGL/GAGL lesions. Similar reverse lesions are seen, as well as unique posterior lesions, such as Bennett and Kim's lesions. When symptoms of apprehension and instability in more than one direction are seen, one should consider multidirectional instability, which often presents with a patulous joint capsule. Finally, owing to significant impacts of daily activities and quality of life, surgical correction of labral tears, bony Bankart defects, Hill Sachs defects, and capsular laxity, may be considered.

Increased nitration of sarcoplasmic reticulum Ca2+-ATPase in human heart failure.

BACKGROUND: Reduced sarcoplasmic reticulum (SR) Ca2+-ATPase (SERCA2a isoform) activity is a major determinant of reduced contractility in heart failure. Ca2+-ATPase inactivation can occur through SERCA2a nitration. We therefore investigated the role of SERCA2a nitration in heart failure. METHODS AND RESULTS: We measured SERCA2a levels and nitrotyrosine levels in tissue from normal and failing human hearts using Western blots. We found that nitrotyrosine levels in idiopathic dilated cardiomyopathic (DCM) hearts were almost double those of control hearts in age-matched groups. Nitrotyrosine was dominantly present in a single protein with the molecular weight of SERCA2a, and immunoprecipitation confirmed that the protein recognized by the nitrotyrosine antibody was SERCA2a. There was a positive correlation between the time to half relaxation and the nitrotyrosine/SERCA2a content (P<0.01) in myocytes isolated from control and DCM hearts. In experiments with isolated SR vesicles from porcine hearts, we also showed that the Ca pump is inactivated by peroxynitrite exposure, and inactivation was prevented by protein kinase A pretreatment. CONCLUSIONS: We conclude that SERCA2a inactivation by nitration may contribute to Ca pump failure and hence heart failure in DCM.

Multifocal visual evoked potentials in the anesthetized non-human primate.

PURPOSE: To evaluate monkey multifocal visual evoked cortical potentials (mfVEPs) recorded from central and peripheral fields for reliability and isolation from electroretinographic (ERG) activity. METHODS: The mfVEP stimulus consisted of a 7-element hexagonal array that subtended 80 degrees of the central visual field. Recordings were made under intravenous pentobarbital sodium (15 mg/kg) anesthesia. Two monkeys with absent optic nerve and ganglion cell function after combined unilateral optic nerve transection and experimental ocular hypertension (ONT/OHT) were followed longitudinally. In a second study, 16 ophthalmologically normal monkeys were tested once. RESULTS: Testing of the non-transected eye in two transected animals revealed robust first- and second-order kernel, first slice (K1 and K2.1) mfVEPs. Stimulation of the transected eye revealed no contamination of the mfVEP from the concurrently recorded multifocal ERGs. There was complete separation of the root-mean-square (RMS) mfVEP amplitudes from the transected and the fellow eyes tested repeatedly across a 4- to 17- month period. The largest amplitude mfVEP was generated by the central element; however, mfVEPs were recorded from outside the central 20 degrees element. The 16 normal animals showed waveforms similar to the normal eyes of the ONT/OHT animals both in shape and distribution throughout the visual field. A scalar-product measure showed both K1 and K2.1 mfVEPs from central and some peripheral elements were statistically distinct from noise. CONCLUSIONS: mfVEPs can be reliably recorded from non-human primates anesthetized with pentobarbital. Under the recording conditions described, mfVEPs are not contaminated by ERG activity. mfVEPs may be useful in animal models of diseases that differentially affect macular and peripheral visual field responsiveness.

Depletion of T-tubules and specific subcellular changes in sarcolemmal proteins in tachycardia-induced heart failure.

OBJECTIVE: The T-tubule membrane network is integrally involved in excitation-contraction coupling in ventricular myocytes. Ventricular myocytes from canine hearts with tachycardia-induced dilated cardiomyopathy exhibit a decrease in accessible T-tubules to the membrane-impermeant dye, di8-ANNEPs. The present study investigated the mechanism of loss of T-tubule staining and examined for changes in the subcellular distribution of membrane proteins essential for excitation-contraction coupling. METHODS: Isolated ventricular myocytes from canine hearts with and without tachycardia-induced heart failure were studied using fluorescence confocal microscopy and membrane fractionation techniques using a variety of markers specific for sarcolemmal and sarcoplasmic reticulum proteins. RESULTS: Probes for surface glycoproteins, Na/K ATPase, Na/Ca exchanger and Ca(v)1.2 demonstrated a prominent but heterogeneous reduction in T-tubule labeling in both intact and permeabilised failing myocytes, indicating a true depletion of T-tubules and associated membrane proteins. Membrane fractionation studies showed reductions in L-type Ca(2+) channels and beta-adrenergic receptors but increased levels of Na/Ca exchanger protein in both surface sarcolemma and T-tubular sarcolemma-enriched fractions; however, the membrane fraction enriched in junctional complexes of sarcolemma and junctional sarcoplasmic reticulum demonstrated no significant changes in the density of any sarcolemmal protein or sarcoplasmic reticulum protein assayed. CONCLUSION: Failing canine ventricular myocytes exhibit prominent depletion of T-tubules and changes in the density of a variety of proteins in both surface and T-tubular sarcolemma but with preservation of the protein composition of junctional complexes. This subcellular remodeling contributes to abnormal excitation-contraction coupling in heart failure.