Explaining variation in perceived team effectiveness: results from eleven quality improvement collaboratives

Aims and objectives. Explore effectiveness of 11 collaboratives focusing on 11 different topics, as perceived by local improvement teams and to explore associations with collaborative‐, organisational‐ and team‐level factors. Background. Evidence underlying the effectiveness of quality improvement collaboratives is inconclusive and few studies investigated determinants of implementation success. Moreover, most evaluation studies on quality improvement collaboratives are based on one specific topic or quality problem, making it hard to compare across collaboratives addressing different topics. Design. A multiple‐case cross‐sectional study. Methods. Quality improvement teams in 11 quality improvement collaboratives focusing on 11 different topics. Team members received a postal questionnaire at the end of each collaborative. Of the 283 improvement teams, 151 project leaders and 362 team members returned the questionnaire. Results. Analysis of variance revealed that teams varied widely on perceived effectiveness. Especially, members in the Prevention of Malnutrition and Prevention of Medication Errors collaboratives perceived a higher effectiveness than other groups. Multilevel regression analyses showed that educational level of professionals, innovation attributes, organisational support, innovative culture and commitment to change were all significant predictors of perceived effectiveness. In total, 27·9% of the individual‐level variance, 57·6% of the team‐level variance and 80% of the collaborative‐level variance could be explained. Conclusion. The innovation’s attributes, organisational support, an innovative team culture and professionals’ commitment to change are instrumental to perceived effectiveness. The results support the notion that a layered approach is necessary to achieve improvements in quality of care and provides further insight in the determinants of success of quality improvement collaboratives. Relevance to clinical practice. Understanding which factors enhance the impact of quality improvement initiatives can help professionals to achieve breakthrough improvement in care delivery to patients on a wide variety of quality problems.     

ACE抑制剂卡托普利对实验性围手术期心肌缺血的影响

目的:图手术期心肌缺血主要是因为应激引起冠状动脉内皮功能障碍所致,所以观察卡托普利对其影响。方法:杂种犬20只均分为4组:Ⅰ组(对照组),Ⅱ组(心肌梗塞模型组),Ⅲ组(心梗 胃大部切除术)和Ⅳ组(心梗 卡托普利 胃大部切除术)。心梗2周后行胃大部分切除术,测定Ⅲ、Ⅳ两组的基础状态、术前和术后的血流动力学指标、血浆内皮素(ET)及一氧化氮(NO)。用组织原位杂交方法观察4组非梗塞区冠脉内皮-氧化氮合酶(NOS)mRNA表达水平。结果:在Ⅲ组,手术使LV dP/dt_(max)、心脏指数(CI)及NO下降,引起LVEDP、PCWP、总外周阻力(TPR)、左室舒张压力下降时间常数(T值)和ET升高。在Ⅳ组,用卡托普利后40min,TPR下降,T值升高;手术使血流动力学指标回降,不影响其它指标。组织原位杂交示,NOS mRNA在Ⅰ组高度表达,Ⅱ组和Ⅳ组次之,Ⅲ组最低。结论:卡托普利能预防胃大部切除术引起的左室舒缩障碍和冠脉内皮功能障碍。     

Identification of human juvenile chronic myelogenous leukemia stem cells capable of initiating the disease in primary and secondary SCID mice

Most juvenile chronic myelogenous leukemia (JCML) cells have limited long-term proliferative capacity, and only a minority of immature cells give rise to colonies in semisolid cultures. Clonogenic JCML progenitors cannot be maintained in culture because they differentiate, and within a few weeks the leukemic clone is lost. This makes it difficult to identify the cell that initiates and maintains the disease in patients. To determine the proliferative capacity of JCML cells in vivo, bone marrow (BM), peripheral blood, or spleen cells from eight patients with JCML either at diagnosis or during treatment were transplanted into sublethally irradiated severe combined immune deficient (SCID) mice. JCML cells from all patients homed to the murine BM and proliferated extensively in response to exogenous stimulation with granulocyte-macrophage colony-stimulating factor. Within a few weeks, highly engrafted mice became ill and cachectic due to infiltration of leukemic cells and secretion of tumor necrosis factor- alpha. Murine BM, spleen, and liver were infiltrated with leukemic blasts, and typical JCML colony-forming progenitors could be recovered. Kinetic experiments demonstrated that only a small minority of transplanted cells homed to the murine BM, and that these cells initiated and maintained the disease in vivo by extensive proliferation and differentiation. To characterize the cell-surface phenotype of the JCML initiating cell (JCML-IC), JCML blood or spleen cells were fractionated on the basis of CD34/CD38 marker expression and transplanted into SCID mice. Only immature CD34+ cells could initiate the disease, while mature CD34- cells did not engraft. Within the CD34+ compartment, there was enrichment for JCML-ICs by immature cells with a CD34+/CD38- stem-cell-like phenotype. Mice transplanted with more mature CD34+/CD38+ populations that also contained clonogenic JCML progenitors were poorly engrafted. These results indicate that the JCML- IC is an earlier stage of development than clonogenic JCML progenitors. Additional evidence that the JCML-IC has stem-cell properties comes from secondary transplant experiments that test the self-renewal capacity. The JCML-IC from all three patients tested could successfully reinitiate the disease in secondary murine recipients. Thus, we have developed a functional in vivo model that replicates many aspects of human JCML, and have used this model to identify and characterize JCML- ICs and their stem-cell properties.     

Observer variability in the histologic assessment of oral premalignant lesions

Histopathologic examination of oral leukoplakias has a major impact on the assessment of prognosis and treatment planning. We investigated the extent of agreement in grading epithelial dysplasia between pathologists with the same or different educational backgrounds. Two general pathologists and two oral pathologists were each given 100 sections of oral leukoplakia to grade from no dysplasia to carcinoma in-situ. The interobserver agreement rates were in the range of 49% to 69%. The calculated kappa values were in the range of 27% to 45%), showing poor to moderate agreement between the pathologists. When comparing the kappa values between the two pairs of pathologists with the same education, these values did not diverge from the general level of kappa values, indicating that the interobserver variability was due to individual differences rather than to educational background.