Introduction Automatic titration modes of non-invasive ventilation, including average volume assured pressure support (AVAPS), are hybrid technologies that target a set volume by automated adjustment of pressure support (PS). These automated modes could offer potential advantages over fixed level PS, in particular, in patients who are super obese. Methods Consecutive patients with obesity hypoventilation syndrome were enrolled in a two-centre prospective single-blind randomised controlled trial of AVAPS versus fixed-level PS using a strict protocolised setup. Measurements The primary outcome was change in daytime arterial PCO 2 (PaCO 2 ) at 3 months. Body composition, physical activity (7-day actigraphy) and health-related quality of life (severe respiratory insufficiency questionnaire, SRI) were secondary outcome measures. Results 50 patients (body mass index 5067 kg/m 2 ; 55611 years; 53% men) were enrolled with a mean PaCO 2 of 6.960.8 kPa and SRI of 53617. 46 patients (23 AVAPS and 23 PS) completed the trial. At 3 months, improvements in PaCO 2 were observed in both groups (AVAPS Δ0.6 kPa, 95% CI 0.2 to 1.1, p<0.01 vs PS Δ0.6 kPa, 95% CI 0.1 to 1.1, p¼0.02) but no betweengroup difference (ΔÀ0.1 kPa, 95% CI À0.7 to 0.6, p¼0.87). SRI also improved in both groups (AVAPS Δ11, 95% CI 6 to 17, p<0.001 vs PS Δ7, 95% CI 1 to 12, p¼0.02; between groups Δ5, 95% CI À3 to 12, p¼0

Augmented Soft Tissue Mobilization (ASTM) is a new non-invasive soft tissue mobilization technique which has been used successfully to treat a variety of musculoskeletal disorders. The purpose of this study was to determine the effects of ASTM therapy on the morphological and functional characteristics of enzyme induced injured rat Achilles tendons. Four groups of five rats were allocated as follows: (A) control, (B) tendinitis, (C) tendinitis plus ASTM, and (D) ASTM alone. Collagenase injury was induced, and the surgical site was allowed to heal for 3 wk. ASTM was performed on the Achilles tendon of groups C and D for 3 min on postoperative days 21, 25, 29, and 33 for a total of four treatments. Gait data were gathered prior to each treatment. The Achilles tendons of each group were harvested 1 wk after the last treatment. Specimens were prepared for light and electron microscopy, and immunostaining for type I and type III collagen and fibronectin was performed. Light microscopy showed increased fibroblast proliferation in the tendinitis plus ASTM treatment group. Although healing in rats may not translate directly to healing in humans, the findings of this study suggest that ASTM may promote healing via increased fibroblast recruitment.

1. Blind analysis of contrast echocardiograms to detect intracardiac shunts, blind analysis of lung function tests for evidence of small airways disease, smoking history and dive characteristics were examined in an attempt to explain neurological symptoms that occurred within 5 min of surfacing from unprovocative dives. 2. Pulmonary abnormalities were significantly more frequent in those divers without intracardiac shunts (50%) than in those with shunts (0%). Smoking was more common in those divers without shunts (55% versus 15%), although this just failed to reach conventional significance levels. Divers without shunts experienced cerebral rather than spinal symptoms after significantly shallower dives with lower tissue nitrogen loads. Depths of dives, tissue nitrogen loads and clinical manifestations in those divers without shunts were similar to the findings in divers who had symptoms after rapid ascents. Despite conservative dive profiles, clinical manifestations in divers with shunts resembled those observed after missed decompression stops. 3. The findings suggest that occult lung disease, and probably smoking, increase the risk of neurological symptoms, even after unprovocative dives, and the similarity of the dive profiles and clinical manifestations to cases with rapid ascents suggest that pulmonary barotrauma and arterial gas embolism are responsible. In divers with intracardiac shunts the different dive profiles and clinical manifestations imply that there is another mechanism, involving different tissue and bubble nitrogen kinetics resulting in venous gas liberation and peripheral amplification in embolized tissues, rather than paradoxical embolism per se.

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