Carleton Lodge, situated on the banks of the Rideau River, is a 160-bed long-term care facility that opened on April 8, 1989. The structure is light wood frame construction with insulated stud walls, vertical aluminum siding, and pitched roof trusses. The Lodge, with a central core and four 2-storey residential wings, has private rooms with en suite bathrooms, which project beyond the face of the main walls, and vent directly outside. There is perimeter hot water heating and ventilation from central make-up air units. Since construction, problems have existed with water infiltration, condensation and mould within the exterior walls. The residential wings were cold and drafty in winter and hot in summer. Whenever mould has been encountered since the building was completed, the City of Ottawa (and formerly the Regional Municipality of Ottawa Carleton) has taken immediate action to remove and remediate and conducted frequent air testing to ensure residents and staff were safe. The project objectives were to solve the problem of water penetration into the exterior walls, carry out mould decontamination, and re-clad with a system that will provide trouble free service with a reasonable degree of maintenance. A holistic approach was applied using integrated design and assessment techniques to investigate and design solutions for the building envelope problems. Remediation considered the possibility of mould, potential for salvaging materials and buildability of the details. A mock up was constructed during the design process to verify constructability and test the improvements to the exterior walls. As residents could not be relocated during construction, the project's greatest challenge was limiting disruption and noise. Construction areas were tarped and negatively pressurized to eliminate dust infiltration. Following exterior inspection and wall reconstruction, interior remediation proceeded on a room-by-room basis and generally without displacing residents. The existing un-vented aluminum cladding assembly with minimal capillary break was replaced with a new rain screen pre-finished aluminum cladding system, consisting of high permeance membrane air/moisture barrier, galvanized z-girts and exterior insulation, new windows, ventilation grilles and dampers, and pre-finished metal siding. Exterior sheathing was improved to act as the primary air barrier, and a continuous thermal barrier was achieved with sprayed on foam insulation at difficult locations. Despite many fixed elements of the building, the project has corrected water penetration problems, decontaminated exterior walls, greatly improved the interior environment, and reduced heating and air conditioning costs. Energy use data is still being collected. Client feedback indicates that the project objectives were achieved.

“Dual-Use policies” are one response to the challenges faced by defence research establishments and defence producers. This article traces the development of Dual-Use Technology Centres (DUTCs), a UK initiative to exploit the capabilities generated in defence research establishments by providing a channel for technology transfer. We find that a number of persistent tensions are creating problems under the current arrangements and conclude that there should be a clear separation within the research organisation of the Ministry of Defence (MoD), between offices concerned with managing research programmes conducted “extra-murally”, and MoD-owned facilities carrying out research.

Although endothelial cell injury and microcirculatory intravascular clotting have been implicated in the pathophysiology of skin-flap failure and various hematologically active drugs have been used to improve flap survival, the basic underlying pathophysiology has not been documented previously. In this study of venous ischemia in pig flaps, we focus on the accumulation and distribution of platelets and fibrinogen in the flap, on the morphologic changes in the flap microcirculation, and on changes in various coagulation factors in the venous effluent from the flap. Bilateral buttock skin flaps and latissimus dorsi myocutaneous flaps were designed and elevated on 12 pigs. All flaps had a primary ischemic insult (clamp application to the vascular pedicle) of 2 hours, followed by 2 hours of reperfusion, and then one side was subjected to a 6-hour period of secondary venous ischemia (clamp application to the dominant flap vein). In six animals, radioactively labeled autologous platelets and human fibrinogen were injected intravenously half an hour before termination of secondary venous ischemia. Flaps were weighed and counted for radioactivity. Flap biopsies and the buffy coat of venous effluent were processed for electron microscopy. In the other six animals, venous effluent was collected before secondary ischemia, upon immediate reperfusion, and at 4 and 8 hours after termination of secondary ischemia. Venous plasma levels of fibrinogen, von Willebrand factor, and antithrombin III were measured. Platelet and fibrinogen accumulation was increased in flaps with venous stasis when compared with control flaps at both time intervals studied; a twofold increase was seen prior to reperfusion, and a threefold increase was seen following 4 hours of reperfusion. Venous effluent could not be collected from buttock skin flaps because of slow reflow and clotting in the collecting system. In comparing the venous effluent of control flaps with that of venous ischemic latissimus dorsi flaps, hematocrit was significantly elevated. Blood samples collected for analysis of fibrinogen, antithrombin III, and von Willebrand factor could not be analyzed because of postcollection clotting. Electron microscopy showed extravasation of red blood cells and activated platelets, fibrin, and red blood cells in distended and partly disrupted capillaries. The venous ischemia reperfusion injury is associated with thrombosis in the microcirculation and alterations in consumption of coagulation factors. This study gives physiologic support for potential beneficial effects of treatment modalities that aim at counteracting the different components of thrombus formation.