Supraacetabular insufficiency fractures

Insufficiency fractures in the supraacetabular region were identified in five women, aged 55-83 years. Factors contributing to the diminished resistance of their bones included postmenopausal osteoporosis, steroid therapy, radiation therapy, and rheumatoid arthritis. The supraacetabular fractures were seen on routine radiographs as hazy bands of sclerosis located immediately above and parallel to the acetabular roof. All five patients had additional fractures in the spine or pelvis. Supraacetabular insufficiency fractures may be an unsuspected cause of hip pain, especially in older women.     

The barium enema appearances in solitary rectal ulcer syndrome

Solitary rectal ulcer syndrome is a benign condition of unknown aetiology, usually found in young adults. The main clinical complaint is of rectal bleeding, often with change in bowel habit. The radiological findings in 17 patients with histologically proven solitary rectal ulcer syndrome, seen at the General Infirmary at Leeds over an 8-year period, are presented. Ulceration, polypoid lesion, stricture, granularity or a normal rectal mucosa may all be found on barium enema. The histological findings and pathogenesis of the condition are discussed.     

Predicting length of hospital stay for psychiatric inpatients

Medicare's use of diagnosis-related groups and the frequent acceptance of length of stay as an indicator of resource utilization has caused a surge of interest in the predictability of length of hospital stay for psychiatric inpatients. By constructing a weighted least squares regression model using data from the 1980 Hospital Discharge Survey, the authors were able to account for an increased amount of variance in length of stay for the major diagnostic categories of mental disorder and substance abuse for Medicare and Blue Cross/Blue Shield patients. The enhanced ability to predict length of stay is attributed to a carefully constructed data base and an increased number of predictor variables, particularly comorbidity. Knowledge of the presence or absence of a chemical dependency unit in the hospitals from which patients were discharged substantially increased the proportion of variance accounted for in the analysis.     

Impaired inhibitory G-protein function contributes to increased calcium currents in rats with diabetic neuropathy

There is a growing body of evidence that sensory neuropathy in diabetes is associated with abnormal calcium signaling in dorsal root ganglion (DRG) neurons. Enhanced influx of calcium via multiple high‐threshold calcium currents is present in sensory neurons of several models of diabetes mellitus, including the spontaneously diabetic BioBred/Worchester (BB/W) rat and the chemical streptozotocin (STZ)‐induced rat. We believe that abnormal calcium signaling in diabetes has pathologic significance as elevation of calcium influx and cytosolic calcium release has been implicated in other neurodegenerative conditions characterized by neuronal dysfunction and death. Using electrophysiologic and pharmacologic techniques, the present study provides evidence that significant impairment of G‐protein‐coupled modulation of calcium channel function may underlie the enhanced calcium entry in diabetes. N‐ and P‐type voltage‐activated, high‐threshold calcium channels in DRGs are coupled to mu opiate receptors via inhibitory G(o)‐type G proteins. The responsiveness of this receptor coupled model was tested in dorsal root ganglion (DRG) neurons from spontaneously‐diabetic BB/W rats, and streptozotocin‐induced (STZ) diabetic rats. Intracellular dialysis with GTPgammaS decreased calcium current amplitude in diabetic BB/W DRG neurons compared with those of age‐matched, nondiabetic controls, suggesting that inhibitory G‐protein activity was diminished in diabetes, resulting in larger calcium currents. Facilitation of calcium current density (I(DCa)) by large‐amplitude depolarizing prepulses (proposed to transiently inactivate G proteins), was significantly less effective in neurons from BB/W and STZ‐induced diabetic DRGs. Facilitation was enhanced by intracellular dialysis with GTPgammaS, decreased by pertussis toxin, and abolished by GDPbetaS within 5 min. Direct measurement of GTPase activity using opiate‐mediated GTPgamma[(35)S] binding, confirmed that G‐protein activity was significantly diminished in STZ‐induced diabetic neurons compared with age‐matched nondiabetic controls. Diabetes did not alter the level of expression of mu opiate receptors and G‐protein alpha subunits. These studies indicate that impaired regulation of calcium channels by G proteins is an important mechanism contributing to enhanced calcium influx in diabetes.