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M B Hill

Publications and source records attributed to M B Hill.

10 recordsLinked to original sources
PubMed2001

Does sharing process differences reduce patient length of stay in the emergency department?

STUDY OBJECTIVE: We assess the ability of the best demonstrated processes (BDP) methodology to decrease emergency department patient length of stay (LOS) in EDs in a large multihospital system. METHODS: Two hundred ninety-one EDs were ranked by LOS, and the fastest and slowest EDs were observed to identify the BDPs. The resulting "meaningful differences" were shared with all EDs throughout the hospital system. LOS studies were repeated after the BDP intervention. Five separate LOS measures were performed during a 19-month period, with 223 to 273 EDs participating in each measure. Three interval times were calculated: arrival to examination room, examination room to physician evaluation, and physician evaluation to discharge. RESULTS: Two hundred ninety-one EDs participated, and 386,837 patient visits were evaluated. Before intervention, the average LOS was 147 minutes for all EDs and 186 minutes in the slowest third. At 19 months after intervention, the average LOS was 139 minutes for all EDs and 157 minutes in the slowest third. Between the initial and final measurement period, there was an 8-minute (5.4%) improvement in LOS on a system-wide basis, and the slowest third of EDs improved LOS by 29 minutes (15.6%). Before intervention, arrival to examination room time was 27 minutes, examination room to physician evaluation was 20 minutes, and evaluation to discharge was 100 minutes. After intervention, these times decreased to 22 (P <.001), 18 (P <.001), and 99 (P =.33) minutes, respectively. The slowest one third of EDs went from 37 to 24 minutes for arrival to examination room time (P <.001), from 25 to 20 minutes for examination room to evaluation time (P <.001), and from 124 to 113 minutes for evaluation to discharge time (P <.001). CONCLUSION: Implementing observed BDP meaningful differences resulted in decreased patient LOS in EDs, particularly in the slowest one third of EDs in the hospital system.

Benchmarking↗
PubMed1998

Anti-endothelial cell antibodies in primary antiphospholipid syndrome and SLE: patterns of reactivity with membrane antigens on microvascular and umbilical venous cell membranes.

Although there has been recent emphasis on autoantibodies to epitopes on beta-2-glycoprotein I and prothrombin in the pathogenesis of antiphospholipid syndrome (APS), antibodies other than those directed toward epitopes on phospholipid binding proteins are present. These include those reactive with antigens on platelet membrane glycoproteins, and with vascular endothelial cell membrane. As the pathogenesis of the thrombotic manifestations of APS remains unexplained, further characterization of these antibodies may be informative. We have confirmed anti-endothelial cell binding to a range of cell membrane antigens in systemic lupus erythematosus (SLE) and primary APS. Furthermore, differences in both the pattern of antibody binding and band intensity between human umbilical vein (HUVEC) and human microvascular endothelial cells (HMEC-1) were demonstrated. Of 17 primary APS sera, antibody binding to HUVEC cell membranes was found in nine and to HMEC-1 membranes in seven. Binding at 72-79 kD was confined to HUVEC. In 32 SLE sera, binding to HUVEC and HMEC-1 membranes was detected in 17 and 22 respectively, binding at 135-155 kD being confined to HMEC-1. These results are consistent with the phenotypic variation in endothelial cells of different origins and confirm the frequent presence of autoantibodies reactive with vascular endothelium in both SLE and PAPS. Whether these antibodies could be involved in the pathogenesis of thrombosis, through induction of endothelial cell apoptosis or damage, remains to be determined.

Adult↗
PubMed1996

Antibodies to membranes of endothelial cells and fibroblasts in scleroderma.

Anti-endothelial and other cell membrane-reactive antibodies in scleroderma were characterized by immunoblotting sera with membrane and cytosol preparations of human umbilical vein endothelial cells (HUVEC), dermal fibroblasts and a T cell lymphoma HUT78. Antibodies reactive with HUVEC membranes were found in 17 of 20 patients with scleroderma (33 bands) in contrast to only two of 20 controls (two bands; P < 0.01) and three of 11 patients with myocardial infarction (four bands). Eleven of the 20 patients possessed antibodies that were specific for HUVEC membrane and did not cross-react with other cell lines. Analysis of patient subgroups showed that HUVEC membrane antibodies were present in nine of 11 patients with systemic sclerosis and in all nine with the CREST syndrome, and were HUVEC-specific in five and six of these cases, respectively. Although considerable heterogeneity was seen, antibodies to an 18-19-kD membrane epitope were found in 11 of the 20 patients but in none of the controls (P < 0.01). This antibody which reacted particularly with HUVEC (n = 9) and HUT78 membranes (n = 9) was associated with CREST syndrome rather than systemic sclerosis (9/9 versus 1/11; P < 0.01), and after elution was shown to possess anticentromere activity. In addition, antibodies reactive with both fibroblast (n = 11; 18 bands) and HUT78 membranes (n = 18; 42 bands) were detected and were specific for either fibroblast or HUT78 membranes in nine and 14 patients, respectively. There was no significant difference in the incidence of these fibroblasts and HUT78 membrane antibodies in the two patient subgroups. These findings support the concept that membrane-reactive antibodies, including anticentromeric antibodies, may play a central role in the pathogenesis of scleroderma, through their ability to react with endothelial cells.

Aged↗
PubMed1996

Further characterization of anti-endothelial cell antibodies in systemic lupus erythematosus by controlled immunoblotting.

Anti-endothelial cell antibodies in systemic lupus erythematosus were further characterized by controlled immunoblotting studies with EN4 defined membrane and cytosol preparations of human umbilical vein endothelial cells. Antibodies to endothelial cell membranes, some of which reacted with the membranes of both dermal fibroblasts and T-cell lymphoma HUT78, were detected in 26/33 patients (78%), but in only 4/34 normal controls (P < 0.001) and 3/11 patients with a recent myocardial infarction. Although the antibody response was very heterogeneous against epitopes ranging from 17 to 205 kDa, there was a tendency to detect particular membrane epitopes at 31-33 kDa (15 cases), 72-78 kDa (eight cases), 66-68 kDa (seven cases) and 17-19 kDa (five cases). No correlations between antibodies to particular epitopes and disease manifestations were observed nor was a relationship to disease activity detected in a retrospective analysis. However, the possibility that anti-endothelial cell antibodies may be pathogenically important was supported by prospective serial studies in two cases with nephritis who showed diminution and disappearance of anti-endothelial cell antibodies as their active disease was treated into remission.

Adult↗
PubMed1995

Characterization and specificity of anti-endothelial cell membrane antibodies and their relationship to thrombosis in primary antiphospholipid syndrome (APS).

Immunoblotting was used to detect antibodies reacting with membrane and cytosol preparations of human umbilical vein endothelial cells (HUVEC), fibroblasts and a T lymphoma line HUT78 in 18 patients with anticardiolipin antibodies (ACA) (14 of whom had had a thrombotic event), 11 patients with a recent myocardial infarction and 17 controls. Multiple membrane-specific antibodies to HUVEC were found in 10 of the patients with ACA (28 bands) and in nine of the patients with thromboses (27 bands) in contrast to only three of the patients with myocardial infarction (four bands) and one control (one band). The most frequently recognized HUVEC membrane epitopes were at 33 kD (four sera), 61-63 kD (five sera) and 76-79 kD (four sera). Although cross-reactivity with fibroblast and/or HUT78 membranes was seen at 33 kD, binding at 61-63 kD and 76-79 kD was specific for endothelial membranes. Although no correlations with the presence and titre of ACA were seen, HUVEC membrane-specific antibodies showed a correlation with venous thrombotic events.

Antibodies, Anticardiolipin↗