The subaqueous margins of calving glaciers have the potential to make significant contributions to glacier mass loss. However, to date, very little is known about the morphology and development of subaqueous margins. A unique combination of sub-bottom profile and bathymetric data collected between 2008 and 2010 in proglacial lakes at Mueller, Hooker and Tasman glaciers in New Zealand’s Southern Alps reveal subaqueous ice ramps extending up to 510 m from the terminus of each glacier. Ice ramp surfaces are undulating and covered with a thick layer (up to 10 m) of unsorted sediment derived from supraglacial and englacial debris, lateral moraines and deltaic deposits. A cyclic calving pattern, relatively stable lake level and the debris cover appear to control the development and maintenance of these ice ramps. High subaerial retreat rates generally correspond to high subaqueous calving rates, although the highest subaerial retreat rates are not associated with the largest ice ramp. Debris mantling the subaqueous ice ramp surfaces insulates the ice from melting and also reduces buoyant forces acting on the terminus. Comparisons with previous studies show that the ice ramps evolve over time with changes in glacier dynamics and water-body properties.

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A 24-year-old man sustained a crush injury to the tibia, which subsequently became infected with Saksenaea vasiformis. He was treated with debridement and a free myocutaneous flap, but amputation was necessary because of mycotic osteomyelitis. S. vasiformis was recovered and identified on the basis of its characteristic morphology on cornmeal agar.

We have found increased small intestinal permeability to 51Cr-ethylenediaminetetra acetate in patients with ankylosing spondylitis compared with controls. There is no significant difference between patients with ankylosing spondylitis and patients with rheumatoid arthritis taking non-steroidal anti-inflammatory drugs (NSAID). The increased intestinal permeability in ankylosing spondylitis is independent ofdisease activity. These findings suggest that the increased permeability is caused by NSAID treatment and is probably not a primary lesion of small bowel mucosa. PATIENTSSeventeen patients with ankylosing spondylitis taking NSAIDs who were attending our rheumatology outpatient clinic were studied. They were compared with two control groups, the first comprising 16 healthy volunteers and the second 19 patients with rheumatoid arthritis being treated with NSAIDs. In our clinical practice we had insufficient patients with ankylosing spondylitis who were not taking NSAIDs to form a separate control group. In these groups, coeliac disease, inflammatory bowel disease, alcohol abuse, and, in the volunteers, NSAID therapy were excluded on the basis ofhistory and clinical examination. The ankylosing spondylitis patients were all men aged 29-63 years, healthy volunteers (eight men and eight women) were aged 24-63 years, and the rheumatoid group (10 men and nine women) were aged 37-82 years. All tests were performed on an outpatient basis and informed consent was obtained before each procedure. METHODSAfter an overnight fast, patients and controls received 150 ml of solution containing 2 g mannitol, 5 g lactulose, 1 g L-rhamnose, 20 g sucrose, 20 g lactose, and 4 MBq of 51Cr-EDTA. The patients' urine was collected for 24 hours after taking the test solution. The collection period was divided into 0-6 hours and 6-24 hours. One ml of thiomersol (10% w/v) was added to the containers as preservative. The addition ofsugars (sucrose and lactose) to the test solution rendered the final solution hyperosmolar at 1200 mOsmol/l.Estimation of urinary recovery of 51Cr-EDTA used the methods described by Bjarnason.56 Urinary L-rhamnose, mannitol, and lactulose were estimated by modification of two gas liquid chromatography methods.910Statistical tests were performed using the Wilcoxon rank sum test, Mann-Whitney U test, and Pearson's correlation test. ResultsWe found that intestinal permeability to 5 Cr-EDTA in the 0-6 hours collection was median 0.35% (range 0.09-0 70) in controls, 0-61% (range 0. 15-1-29) in ankylosing spondylitis and 0 54% (range 0. 12-1.27) in rheumatoid arthritis. In the 6-24 hours collection values were: median 1.23% (range 0@43-21) control; 1.31% (0 3-2.28) ankylosing spondylitis, and 2.12 (0-12-11-40) rheumatoid arthritis. The sugar permeability results were: lactulose 0.25% (0.05-1 1), rhamnose 8-6% (4 9-24 9), and lactulose/ rhamnose (L/R) ratio 0.02 (0.01-0.05) in controls; lactulose 0-26% (0.04-0 59), rhamnose 8-8% (1-2-11-6), and L/R ratio 0.03 (0-01-0-27) in ankylosing spondylitis; and lactulose 0...

It is known that some cases of neural crest tumours are hereditary. We report the clinical and cytogenetic findings in a three-generation, extended family, four members of which developed single or multiple neural crest tumours (ganglioneuroma, ganglioneuroblastoma or neuroblastoma). To our knowledge, this is the first report of a family with three generations affected. No constitutional cytogenetic abnormality was found in the two members tested. We also review the literature on familial neural crest tumours, with emphasis on those affecting more than one generation. It is important that a detailed family history, with particular reference to tumours, is obtained in all cases of childhood cancer.