A test of your skills.
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Biomedical subjects
Publications and source records attributed to M Bennett.
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A small body of literature has been published reporting the application of topical oxygen for chronic non-healing wounds . Frequently, and erroneously, this form of oxygen administration has been referred to as "topical hyperbaric oxygen therapy" or even more erroneously "hyperbaric oxygen therapy." The advocates of topical oxygen claim several advantages over systemic hyperbaric oxygen including decreased cost, increased safety, decreased complications and putative physiologic effects including decreased free radical formation and more efficient delivery of oxygen to the wound surface. With topical oxygen an airtight chamber or polyethylene bag is sealed around a limb or the trunk by either a constriction/tourniquet device or by tape and high flow (usually 10 liters per minute) oxygen is introduced into the bag and over the wound. Pressures just over 1.0 atmospheres absolute (atm abs) (typically 1.004 to 1.013 atm abs) are recommended because higher pressures could decrease arterial/capillary inflow. The premise for topical oxygen, the diffusion of oxygen into the wound adequate to enhance healing, is attractive (though not proven) and its delivery is certainly less complex and expensive than hyperbaric oxygen. When discussing the physiology of topical oxygen, its proponents frequently reference studies of systemic hyperbaric oxygen suggesting that mechanisms are equally applicable to both topical and systemic high pressure oxygen delivery. In fact, however, the two are very different. To date, mechanisms of action whereby topical oxygen might be effective have not been defined or substantiated. Conversely, cellular toxicities due to extended courses of topical oxygen have been reported, although, again these data are not conclusive, and no mechanism for toxicity has been examined scientifically. Generally, collagen production and fibroblast proliferation are considered evidence of improved healing, and these are both enhanced by hyperbaric oxygen therapy. Paradoxically, claims of decreased collagen production and fibroblast inhibition in wounds subjected to topical oxygen have been reported in studies of topical oxygen as a benefit of topical oxygen therapy. The literature on topical oxygen is mostly small case series or small controlled but not randomized trials. Moreover, the studies generally are not aimed at specific ulcer types, but rather at "chronic wounds." This non-specific approach is recognized as a major design flaw in any study of therapies designed to improve impaired wound healing. The only randomized trial for topical oxygen in diabetic foot ulcers actually showed a tendency toward impaired wound healing in the topical oxygen group. Contentions that topical oxygen is superior to hyperbaric oxygen are not proven. There are potentially plausible mechanisms that support both possibly beneficial and detrimental effects of topical oxygen therapy, and thus well designed and executed basic science research and clinical trials are clearly needed. There is some ongoing research in regard to the role of topical oxygen at established wound laboratories. Neither CMS nor other third party payors recognize or reimburse for topical oxygen. Therefore, the policy of the Undersea and Hyperbaric Medical Society in regard to topical oxygen is stated as follows: 1. Topical oxygen should not be termed hyperbaric oxygen since doing so either intentionally or unintentionally suggests that topical oxygen treatment is equivalent or even identical to hyperbaric oxygen. Published documents reporting experience with topical oxygen should clearly state that topical oxygen not hyperbaric oxygen is being employed. 2. Mechanisms of action or clinical study results for hyperbaric oxygen cannot and should not be co-opted to support topical oxygen since hyperbaric oxygen therapy and topical oxygen have different routes and probably efficiencies of entry into the wound and their physiology and biochemistry are necessarily different. 3. The application of topical oxygen cannot be recommended outside of a clinical trial at this time based on the volume and quality of scientific supporting evidence available, nor does the Society recommend third party payor reimbursement. 4. Before topical oxygen can be recommended as therapy for non-healing wounds, its application should be subjected to the same intense scientific scrutiny to which systemic hyperbaric oxygen has been held.
A recent workshop found that with no-decompression dives, "reversed dive profiles" (RDP) did not increase the risk of decompression sickness (DCS). Thus in multi-level dives, the deeper part of a dive may be performed later in the dive, and repetitive dives may progress from shallow to deep. This contradicts the conventionally recommended forward dive profile (FDP) when the deeper dive, or deeper part of the dive, is performed first. The RDP Workshop recommendations were made despite the absence of adequate data. We performed two groups of experiments to test this hypothesis. We exposed two matched groups of 11 guinea pigs each to forward and reverse multi-level diving profiles to determine any substantial difference between FDPs and RDPs. There was no evidence of DCS in any of the FDP animals, while six (55%) of the RDP animals exhibited symptoms of severe DCS and died. This difference was statistically significant (P = 0.01). We then compressed two groups each of 11 guinea pigs to repetitive dives to determine any substantial difference in the risk of DCS when two equivalent sets of three dives were conducted from the deepest to most shallow on the one hand (FDP), and from the shallowest to the deepest on the other (RDP). Over two such series of dives (the second extended in time and depth to increase DCS risk), there was a significantly higher incidence of severe DCS in those animals in the RDP group. Seven of 21 exposures (33%) in the RDP group resulted in severe DCS versus none in the FDP group (P = 0.01). Our findings suggest that multi-level and repetitive dives performed in the established FDP manner are less hazardous than those performed in the reverse profile mode, at least for the exposures we chose. We believe the recommendations of the workshop should be re-examined.
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A neuropathologic study of 100 patients with fatal head injuries admitted to a neurosurgical unit revealed hypoxic-ischaemic brain damage in 74% and diffuse axonal injury in 42% of patients respectively. Of the seven patients who died as a result of extracerebral injuries, there were four in whom death due to hypovolaemic shock, was considered potentially avoidable. This study indicates that there is scope for improvement in the management of patients with acute head injury, particularly in the prevention of secondary brain damage, and in the need to increase awareness of potentially life threatening extracerebral injuries as a cause of coma.
In all areas of nursing, the concept of caring encompasses the core of our practice and is the outcome of skilled practitioners. In occupational health nursing (OHN) it is no different. 'Caring' has been described by many authors, used in theoretical models of nursing and forms the basis of much research. This paper looks at the provision of care in the OH setting within Northern Ireland, with particular reference to problems which have arisen from the troubles.
(C57BL/6 x DBA/2)F1 mice were fed antioxidant-matched fish oil (FO) or corn oil (CO) diets for weeks, were challenged with B16.F10 melanoma cells, and lung metastases were enumerated 17 days later. Mice fed FO had fewer lung tumors than mice fed CO. This dietary effect persisted in mice injected with monoclonal antibodies which depleted natural killer cells, CD8+ T cells or CD4+ T cells. Generation of specific anti-B16.F10 cytotoxic cells in vitro by splenocytes from immunized mice was greater in mice fed FO. Even though host resistance to lung metastases by B16.F10 cells is mediated in large part by natural killer cells, CO and/or FO may have affected cells not tested here or tumor cells themselves.
Strains of mice differ greatly in resistance to infection in their lungs with virulent Mycoplasma pulmonis (MP) organisms even during the first 5 days, prior to detection of humoral or T cell mediated acquired immune responses. C57BL/6 mice are resistant, and BALB/c and C3H mice are susceptible, and one major gene, MP, not linked to the H2 major histocompatibility complex, regulates resistance. C57BL/6 x C3H (B x H) and BALB/c x C57BL/6 (C x B) recombinant inbred strain mice were infected intratracheally with the T2 strain of MP. Five days later, the recovery of organisms from tracheolung lavages and lung tissue was determined. The strain distribution pattern of resistance indicated that the MP gene maps to chromosome 4. B6.C-H18 (B6 mice congenic for the BALB/c H18 gene of chromosome 4) were much more susceptible than B6 mice, but were less susceptible than BALB/c mice, supporting the data obtained with the recombinant inbred strain mice, but suggesting that other genes may also influence resistance to infection with MP.