Barriers to detecting and treating hypercholesterolaemia in patients with ischaemic heart disease: primary care perceptions

BACKGROUND: Treating hypercholesterolaemia in patients with ischaemic heart disease can significantly reduce vascular deaths and events. Many such patients, however, do not receive effective treatment for hypercholesterolaemia. AIM: To ascertain the barriers to the detection and treatment of hypercholesterolaemia in patients with ischaemic heart disease as seen by primary care teams. DESIGN OF STUDY: Qualitative study using the nominal group technique. SETTING: General practice teams in the North Thames region of the Medical Research Council General Practice Research Framework. METHOD: The main outcomes measures used were identification of the barriers to the detection and treatment of hypercholesterolaemia together with relative rankings. RESULTS: Fourteen individual barriers were identified. The main barriers were: organisational barriers within general practices; confusing and conflicting guidelines from external sources; errors and omissions by GPs; communication problems at the interface between secondary and primary care; and reluctance by patients to take medication. CONCLUSIONS: The reasons for suboptimal detection and treatment of hypercholesterolaemia are complex and act at various levels. Interventions to improve the management of this condition must address these barriers in order to be successful.     

Extracorporeal CO2 Removal in severe adult respiratory distress syndrome

Sixty-five per cent survival has been achieved in a group of patients with severe ARDS and a predicted mortality of 92%, by the use of Gattinoni's technique of extracorporeal CO2 removal. In patients and animals the technique has usually resulted in rapid improvement in the radiographic appearance and lung function. There are several possible mechanisms by which the technique may facilitate lung repair, including improvement of lung tissue oxygenation, the avoidance of high airway pressures and regional alkalosis in the lung, a reduction in oxygen toxicity, and the frequency observed reduction in pulmonary artery pressure. The apparent effectiveness of the technique and other associated evidence have implications which should lead us to reconsider some aspects of our conventional management of patients with severe ARDS.     

高效液相色谱法测定炎痛净乳膏中双氯芬酸钠和苯佐卡因的含量

目的：测定炎痛净乳膏中双氯芬酸钠和苯佐卡因的含量。方法：高效液想象以谱法，甲醇为提取溶剂，地西泮为内标，No-va-PakC18色谱柱，甲醇-水-冰醋酸（80：20：0.5)为流动相，检测波长为283nm。结果：双氯芬酸钠和苯佐卡因在5μg/ml-40μg/ml范围内，其浓度与峰面积均呈良好的线性关系（r=0.9999)，平均回收率分别为101.0%,RSD=1.21%,99.8%,RSD=0.62%。结论：本法专属性强，操作简便，结果准确。     

H-2-restricted cytotoxic effectors generated in vitro by the addition of trinitrophenyl-conjugated soluble proteins

Murine spleen cells from normal donors were cultured in vitro with trinitrobenzene sulfonate (TNBS)-conjugated soluble proteins, i.e., bovine gamma globulin (TNP-BGG) or bovine serum albumin (TNP-BSA). Addition of 100 μg of any of these TNP-proteins to the spleen cell cultures led to the generation of cytotoxic T-cell effectors which were H-2-restricted and TNP- specific. The lytic potential of such effectors was comparable to that generated by sensitization with TNBS-modified syngeneic cells, and was restricted to haplotypes shared at the K or K plus I-A, or the D regions of the H-2 complex. Greater effecter cell activity was generated by addition of TNP-BGG against TNBS-modified targets which shared K plus I-A than against modified targets which shared the D region with the responding cells, which suggests that the same immune response genes are involved when the response is generated by the addition of TNP-conjugated soluble proteins or of TNBS- modified cells. H-2-restricted, TNP-specific effecter cells were generated by culturing mouse spleen cells with syngeneic cells which had been preincubated with TNP- BGG or TNP-BSA for 1.5 h. The addition of unconjugated soluble proteins to the cultures did not result in cytotoxic effectors detectable on H-2-matched targets, whether the targets were prepared by modification with TNBS, or by incubation with either the unconjugated or TNP-conjugated proteins. Depletion of phagocytic cells in the tumor preparation by Sephadex G-10 column fractionation before incubation with TNP-BSA had no effect on their lysis by the relevant effector cells. Immunofluorescent staining of tumor target cells with anti-TNP antibodies indicated that TNP could be detected on the tumor cells within 10 rain of incubation with TNP-BSA. The cytotoxic response generated by addition of the TNP-proteins to spleen cell cultures was found to be T-cell dependent at the effector phase, as shown by the sensitivity of the lytic phase to absorbed RAMB and complement. Furthermore, the response did not appear to be attributable to antibody-dependent cellular cytotoxicity. Three mechanisms were considered which could account for the generation of H-2-restricted, TNP-specific, cytotoxic T-cell effectors by the addition of soluble TNP-proteins. These include covalent linkage of activated TNP groups from the soluble proteins to cell surface components, macrophage processing of the soluble conjugates and presentation to the responding lymphocytes in association with H-2-coded self structures, or hydrophobic interaction of the TNP-proteins to cell surfaces. Results obtained from sodium dodecyl sulfate gel patterns indicating that cell-bound TNP was still linked to BSA, and the observation that phagocytic-depleted cells could interact with the soluble TNP-proteins and function as H-2-restricted targets, appear not to favor the first two proposed mechanisms.