Publications by authors named "McGEORGE M"

Objective: This paper explores the use of pharmacoeconomic methods of valuation to health impacts resulting from exposure to poor air quality. In using such methods, interventions that reduce exposure to poor air quality can be directly compared, in terms of value for money (or cost-effectiveness), with competing demands for finite resources, including other public health interventions.

Design: Using results estimated as part of a health impact assessment regarding a West Yorkshire Low Emission Zone strategy, this paper quantifies cost-saving and health-improving implications of transport policy through its impact on air quality.

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Background: The lack of a consistent model means that the quality and characteristics of memory services can vary greatly. Quality standards have been successfully applied in a range of healthcare settings which allow services to implement improvements where necessary. A nationally agreed set of quality standards would help fulfil this need for UK memory services.

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Objective: To evaluate clinical and cost effectiveness of implementing evidence-based guidelines for the prevention of stroke.

Design: Cluster-randomised trial

Setting: Three primary care organisations in the North of England covering a population of 400,000.

Participants: Seventy six primary care teams in four clusters: North, South & West, City I and City II.

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Problem: Rapid referral and management of patients with transient ischaemic attacks is a key component in the national strategy for stroke prevention. However, patients with transient ischaemic attacks are poorly identified and undertreated.

Design And Setting: Before and after evaluation of quality improvement programme with controlled comparison in three primary care trusts reflecting diverse populations and organisational structures in an urban district in the North of England.

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Previous reports have suggested that Lewis (Le) antigens may exert a significant effect on cadaver renal allograft (CRA) survival, especially in black recipients in whom there is a higher frequency of Le-negative phenotypes. We review our experience with this problem in 70 donor-recipient pairs of CRA who underwent prospective Le typing and received conventional immunosuppression between 1980 and 1983. Recipient typing alone yielded the following graft survival (GS) and patient survival (PS) at 2 years by life table analysis: (a+,b;-) (n = 12) 51% GS, 93% PS; (a-, b+) (n = 44) 57% GS, 88% PS; and (a-,b-) (n = 14) 51% GS, 93% PS(P-ns for GS, PS).

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The experience at a single center with 297 consecutive cadaver renal transplants over the past 12 years is reviewed with special attention to acute post-transplant ischemic renal injury (ATN). Sixty-seven patients received kidneys which failed to function immediately (22.5 per cent).

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Eighty-four recipients of cadaveric renal allografts were retrospectively crossmatched for donor-specific pretransplant B cell antibody. Of these, 28 were found to be positive for the antibody and 56 were negative. Actuarial survival analysis over six years revealed a slightly better graft survival overall in the B-cell-negative group as compared with the B-cell-positive group (P less than 0.

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Total lymphoid irradiation (TLI) has been shown to have a strong immunosuppressive effect both experimentally and clinically. Pretransplant blood transfusions have also been shown to have a strong beneficial effect in the outcome of organ transplantation. A study was made of the effect of TLI and pretransplant blood transfusions, alone and in combination, as an immunosuppressive modality in the isolated pancreatic islet transplant in the rat model.

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Twenty-five children with acute lymphoblastic leukemia (ALL) were tested for natural killer (NK) and K-cell activity in vitro using the nonsensitized myeloid/erythroid cell line K562 and the K562 sensitized with rabbit antithymocyte globulin, respectively. The patients consisted of two groups: 1) 13 patients in continuous first remission undergoing maintenance chemotherapy and 2) 12 patients in remission for at least five years in whom chemotherapy had been discontinued at least six months before this study. The first group consistently demonstrated a marked depression in their NK activity and antibody-dependent cell-mediated cytotoxicity (K-cell activity), as compared with normal controls.

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Peritoneal macrophages from mice infected with herpes simplex virus type 2 (HSV-2) exhibited extrinsic antiviral resistance. When the macrophages were co-cultivated in vitro with virus-infected cells the yield of virus was reduced markedly. Activity was not present 1 to 2 days p.

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Pretreatment of mice intraperitoneally with silica, trypan blue, or dextran sulfate to inhibit macrophage function markedly increased the lethality of a systemic intravenous infection with herpes simplex virus type 2, but did not affect the lethality or local virus growth after vaginal infection of mice with herpes simplex virus type 2. Agents which inhibit macrophage function by different mechanisms decreased host resistance to herpes simplex virus type 2, but the effects of macrophage-inhibitory agents may vary according to the route of virus infection.

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Relationships among cell-mediated immune (CMI) responses, neutralizing antibody, and macrophages in host resistance to vaginal or systemic infection with HSV-2 were defined in BALB/c mice. The importance of T-lymphocytes in resistance to either systemic or vaginal infection was demonstrated by increased susceptibility of mice depleted of T-lymphocytes. A role for non-specific resistance against the systemic, but not vaginal, infection was demonstrated by increased susceptibility of mice depleted of macrophages.

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The temporal relationships among the humoral and cellular immune responses were defined in BALB/c mice after vaginal or systemic infection with herpes simplex virus type 2 (HSV-2). After vaginal infection, mice showed evidence of clinical vaginitis on days 4 to 6 and HSV-2 replication was detected locally in the vaginal secretions, cervix, vagina, and uterus before the virus subsequently spread to the central nervous system. Death from encephalitis occurred between 7 and 10 days after infection.

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