Pituitary fossa: chemical shift effect in MR imaging

The effect of chemical shift on magnetic resonance (MR) imaging of the pituitary fossa was studied. Healthy volunteers underwent conventional MR imaging of the pituitary fossa and then imaging with the frequency-encoding gradient reversed or with the phase- and frequency-encoding gradients interchanged. Comparison of the image pairs in each subject showed that the thin, black stripe evident at the water-fat interface within the pituitary fossa was altered when the gradients were changed. Therefore, the low-intensity signal within the pituitary fossa is a chemical shift misregistration effect.     

Anulus fibrosus in bulging intervertebral disks

In this investigation the association of radial tears of the anulus fibrosus and bulging of the intervertebral disk was studied. An index of disk bulging was measured in sagittal anatomic sections in 149 lumbar disks from 31 cadavers. The indexes of disk bulging were correlated with stages of disk development and the presence of an annular tear. The largest disk-bulging indexes were always associated with radial tears of the anulus. Eighty-four percent of the disks with radial tears had disk-bulging indexes greater than 2.5 mm. Most normal adult disks had an index of less than 2.5 mm. The results challenge the concept that the anulus fibrosus is intact in bulging disks, although ruptured in herniated disks.     

Osteopetrosis: MR characteristics at 1.5 T

Four patients with proved osteopetrosis (three with the infantile malignant form and one with the benign form) were examined with magnetic resonance imaging at 1.5 T. All patients were studied in the coronal and sagittal planes using both short and long repetition time/echo time sequences. The infantile malignant form was characterized by a complete lack of signal from the marrow alternating with a signal intensity equivalent to that of the intervertebral disks, resulting in a "stepladder" appearance. In the benign form or after successful marrow transplantation in the infantile malignant form, intermediate or high signal intensity in the vertebrae was noted, suggesting the presence of some marrow elements.     

Treatment of vesico-ureteric reflux in children with neuropathic bladder: a comparison of surgical and endoscopic correction

BACKGROUND/PURPOSE: Vesico-ureteric reflux (VUR) is a common problem in children with neuropathic bladder. Lesser-degree VUR may be manageable by intermittent catheterization or by anticholinergics, but higher grades usually require surgical treatment. If left untreated, two thirds of such patients may experience deterioration of the upper renal tracts. The aim of this study was to compare the results of the STING (Subureteric Teflon Injection) technique with surgical ureteric reimplantation as treatment for VUR in neuropathic bladder. METHODS: From January 1981 to December 1996, 58 children with NB (81 ureters) were treated for VUR. STING and Cohen ureteroneocystotomy were performed in 40 and 41 ureters, respectively. Mean age was 4.5 years (STING) and 5.1 years (Cohen). RESULTS: Twenty-nine of 40 refluxing ureters (72.5%) were cured by STING, whereas Cohen eradicated reflux in 39 of 41 ureters (95.5%). No complications were observed in either group. All the ureters in which STING failed were treated successfully by Cohen ureteroneocystostomy. The 2 ureters still refluxing after surgical reimplantation were cured successfully by a single STING. The mean follow-up was 6.8 years in the Cohen group and 4.8 years in the STING group. During follow-up, no recurrence was observed in patients cured by open reimplantation. In the STING group, 2 previously cured ureters showed recurrence of VUR: both were treated successfully by a further STING. CONCLUSIONS: Open ureteral reimplantation is more effective than STING in correcting VUR in children with neuropathic bladder dysfunction. Nevertheless, the good success rate, the relative technical simplicity, outpatient nature, and rapid recovery point to STING as a safe and effective procedure for the initial treatment of VUR. Failure of STING does not preclude a successful open operation.     

Activation of factor XI in plasma is dependent on factor XII [see comments]

The activation of factor XI initiates the intrinsic coagulation pathway. Until recently it was believed that the main activator of factor XI is factor XIIa in conjunction with the cofactor high molecular weight kininogen on a negatively charged surface. Two recent reports have presented evidence that in a purified system factor XI is activatable by thrombin together with the soluble polyanion dextran sulfate. To assess the physiological relevance of these findings we studied the activation of factor XI in normal and factor XII-deficient plasma. We used either kaolin/cephalin or dextran sulfate as a surface for the intrinsic coagulation pathway, tissue factor to generate thrombin via the extrinsic pathway, or the addition of alpha-thrombin directly. 125I-factor XI, added to factor XI-deficient plasma at physiologic concentrations (35 nmol/L), is rapidly cleaved on incubation with kaolin. The kinetics appear to be exponential with half the maximum cleavage at 5 minutes. Similar kinetics of factor XI cleavage are seen when 40 nmol/L factor XIIa (equal to 10% of factor XII activation) is added to factor XII-deficient plasma if an activating surface is provided. Tissue factor (1:500) added to plasma did not induce cleavage of factor XI during a 90-minute incubation, although fibrin formation within 30 seconds indicated that thrombin was generated via the extrinsic pathway. Adding 1 mumol/L alpha-thrombin (equivalent to 50% prothrombin activation) directly to factor XII deficient or normal plasma (with or without kaolin/cephalin/Ca2+ or dextran sulfate) led to instantaneous fibrinogen cleavage, but again no cleavage of factor XI was observable. We conclude that in plasma surroundings factor XI is not activated by thrombin, and that proposals of thrombin initiation of the intrinsic coagulation cascade are not supportable.