Pachymeningeal enhancement, synonymous with dural enhancement, is a radiological feature best appreciated on a contrast-enhanced magnetic resonance imaging (MRI). The vasculature of the dura mater is permeable, facilitating avid uptake of contrast agent and subsequent enhancement. Thin, discontinuous enhancement can be normal, seen in half the normal population. In patients complaining of postural headaches worse on sitting, gadolinium-enhanced MRI findings of diffuse pachymeningeal enhancement is highly suggestive of benign intracranial hypotension. In these cases, the process of pachymeningeal enhancement is explained by the Monro-Kellie doctrine as compensatory volume changes by vasocongestion and interstitial oedema of the dura mater due to decreased cerebrospinal fluid (CSF) pressure. Focal and diffuse pachymeningeal enhancement can also be attributed to infectious or inflammatory, neoplastic and iatrogenic aetiologies. Correction of the underlying pathology often results in spontaneous resolution of the pachymeningeal enhancement. There have also been reports of pachymeningeal enhancement associated with cerebral venous sinus thrombosis, temporal arteritis, baroreceptor reflex failure syndrome and arteriovenous fistulae.
We present an unusual and rare complication caused by gastric band erosion into the stomach after band placement 15 years ago. The complication was only picked up after the band had subsequently migrated from the stomach at the site of erosion, to the distal ileum causing acute small bowel obstruction and focal perforation requiring emergency laparotomy.Abdominal pain in patients with gastric band should always be treated as serious until proven otherwise.
1. The fluorescent dye 3,3'-dipropyloxadicarbocyanine was used to show that the tumour cells absorbed 2-aminoisobutyrate, glycine, L-leucine and L-isoleucine and certain other amino acids electrogenically. The Km values with respect to amino acid concentration ([A]o), obtained from the fluorescence assays, varied through the above series from 0.8 to 26 mM, with Vmax. fairly constant. 2. Similar Km values described the uptake of the 14C-labelled amino acids in five instances where this was measured. 3. Each amino acid lowered the membrane potential (E) by 10-20 mV when its cellular concentration ([A]i) had reached a steady value and [A]o was 10mM. In these experiments energy metabolism was maintained by glycolysis, 2,4-dinitrophenol was present and cellular respiration was inhibited. The corresponding net flow of amino acid through the Na+ symport was deduced by making use of the fact that the depolarization an amino acid initially caused was roughly proportional to the net influx of amino acid itself. 4. The steady-state depolarization was attributed to the presence of a leak pathway for the amino acid with a rate coefficient PA. As assayed in the absence of Na+, PA was about 5-fold larger for isoleucine than for glycine. 5. Direct estimates of Vmax./PA were similar to those inferred from the extent of depolarization in the steady state and [A]i. 6. A mathematical model was used to predict [A]i/[A]o in term of the measured values of [Na]o, [Na]i, E, Km and Vmax./PA. The predicted and observed values agreed fairly well when [A]o was 1 mM or 10 mM. 7. [A]i/[A]o varied from about 2.5 for 10 mM-isoleucine to 30 for 1 mM-2-aminoisobutyrate when delta microNa, expressed as a ratio, was ostensibly in the range 19-43. 8. The concentration of 2-aminoisobutyrate from a 0.1 mM solution in the presence or absence of ouabain was consistent with the model, whereas the concentration of isoleucine from a 0.1 mM solution exceeded the predicted values 2-5-fold. 9. The tumour cells concentrated 2-amino-bicyclo[2,2,1]heptane-2-carboxylic acid by a non-electrogenic mechanism, with which isoleucine may also interact.
Parenchymal and vascular image qualities, as well as subjective image quality assessments, were equal or superior in comparison to non-split-bolus multi-phase trauma CT protocols. Split-bolus single-pass CT decreased radiation exposure in all studies. Further research is required to determine the superior split-bolus protocol and the specificity and sensitivity of detecting blunt cerebrovascular injury screening, splenic parenchymal vascular lesions, and characterization of pelvic vascular extravasation.
We conclude that patients with prostheses with excellent long-term clinical results as validated by joint registries, routine follow-up of asymptomatic THA should be questioned and requires further investigation. Based on the work of this study, the current practice of routine follow-up of asymptomatic THA may be excessively costly and unnecessary, and a less resource-intensive review method may be more appropriate.
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