Re-engineering the operating room using variability methodology to improve health care value.

BACKGROUND: Variability in flow of patients through operating rooms has a dramatic impact on a hospital's performance and finances. Natural variation (uncontrollable) and artificial variation (controllable) differ and require different resources and management. The aim of this study was to use variability methodology for a hospital's surgical services to improve operational performance. STUDY DESIGN: Over a 3-month period, all operations at a referral center were classified as either scheduled (artificial variation) or unscheduled (natural variation). Data regarding patient flow were collected for all cases. From these data, mathematical models determined explicit resources to be allocated for scheduled and unscheduled cases, with isolation of the 2 flow streams. Services were allocated block time based on 80% prime time use, and scheduled cases were capped at 5:00 PM. Guidelines for operating room access were implemented to smooth the daily schedule and minimize artificial variation on the day of surgery. After implementation of this redesign, 12 months of data were compared with the previous 12-month period. Metrics analyzed included prime time use, overtime minutes, access for urgent or emergent cases, the number of room changes to the elective schedule on the day of surgery, and variation of daily schedules. RESULTS: Surgical volume and surgical minutes increased by 4% and 5%, respectively. Prime time use increased by 5%. Overtime staffing decreased by 27%. Day-to-day variability decreased by 20%. The number of elective schedule same day changes decreased by 70%. Staff turnover rate decreased by 41%. Net operating income and margin improved by 38% and 28%, respectively. CONCLUSIONS: Variability management results in improvement in operating room operational and financial performance. This optimization may have a significant impact on a hospital's ability to adapt to health care reform.

SPAM-MQ-HETCOR: an improved method for heteronuclear correlation spectroscopy between quadrupolar and spin-1/2 nuclei in solid-state NMR.

The recently introduced concept of soft pulse added mixing (SPAM) is used in two-dimensional heteronuclear correlation (HETCOR) NMR experiments between half-integer quadrupolar and spin-1/2 nuclei. The experiments employ multiple quantum magic angle spinning (MQMAS) to remove the second order quadrupolar broadening and cross polarization (CP) or refocused INEPT for magnetization transfer. By using previously unexploited coherence pathways, the efficiency of SPAM-MQ-HETCOR NMR is increased by a factor of almost two without additional optimization. The sensitivity gain is demonstrated on a test sample, AlPO(4)-14, using CP and INEPT to correlate (27)Al and (31)P nuclei. SPAM-3Q-HETCOR is then applied to generate (27)Al-(31)P spectra of the devitrified 41Na(2)O-20.5Al(2)O(3)-38.5P(2)O(5) glass and the silicoaluminophosphate ECR-40. Finally, the method allowed the acquisition of the first high resolution solid-state correlation spectra between (27)Al and (29)Si.

cTnT1, a cardiac troponin T isoform, decreases myofilament tension and affects the left ventricular pressure waveform.

Four isoforms of cardiac troponin T (cTnT), a protein essential for calcium-dependent myocardial force development, are expressed in the human; they differ in charge and length. Their expression is regulated developmentally and is affected by disease states. Human cTnT (hcTnT) isoform effects have been examined in reconstituted myofilaments. In this study, we evaluated the modulatory effects of overexpressing one cTnT isoform on in vitro and in vivo myocardial function. A hcTnT isoform, hcTnT(1), expressed during development and in heart disease but not in the normal adult heart, was expressed in transgenic (TG) mice (1-30% of total cTnT). Maximal active tension measured in skinned myocardium decreased as a function of relative hcTnT(1) expression. The pCa at half-maximal force development, Hill coefficient, and rate of redevelopment of force did not change significantly with hcTnT(1) expression. In vivo maximum rates of rise and fall of left ventricular pressure decreased, and the half-time of isovolumic relaxation increased, with hcTnT(1) expression. Substituting total cTnT charge for hcTnT(1) expression resulted in similar conclusions. Morphometric analysis and electron microscopy revealed no differences between wild-type (non-TG) and TG myocardium. No differences in isoform expression of tropomyosin, myosin heavy chain, essential and regulatory myosin light chains (MLC), TnI, or in posttranslational modifications of mouse cTnT, cTnI, or regulatory MLC were observed. These results support the hypothesis that cTnT isoform amino-terminal differences affect myofilament function and suggest that hcTnT(1) expression levels present during human development and in human heart disease can affect in vivo ventricular function.

Adult-derived liver stem cells acquire a cardiomyocyte structural and functional phenotype ex vivo.

We examined the differentiation potential of an adult liver stem cell line (WB F344) in a cardiac microenvironment, ex vivo. WB F344 cells were established from a single cloned nonparenchymal epithelial cell isolated from a normal male adult rat liver. Genetically modified, WB F344 cells that express beta-galactosidase and green fluorescent protein or only beta-galactosidase were co-cultured with dissociated rat or mouse neonatal cardiac cells. After 4 to 14 days, WB F344-derived cardiomyocytes expressed cardiac-specific proteins and exhibited myofibrils, sarcomeres, and a nascent sarcoplasmic reticulum. Further, rhythmically beating WB F344-derived cardiomyocytes displayed calcium transients. Fluorescent recovery after photobleaching demonstrated that WB F344-derived cardiomyocytes were coupled with adjacent neonatal cardiomyocytes and other WB F344-derived cardiomyocytes. Fluorescence in situ hybridization experiments suggested that fusion between WB F344 cells and neonatal mouse cardiomyocytes did not take place. Collectively, these results support the conclusion that these adult-derived liver stem cells respond to signals generated in a cardiac microenvironment ex vivo acquiring a cardiomyocyte phenotype and function. The identification ex vivo of microenvironmental signals that appear to cross germ layer and species specificities should prove valuable in understanding the molecular basis of adult stem cell differentiation and phenotypic plasticity.