Measuring hospital efficiency with frontier cost functions

This paper uses a stochastic frontier multiproduct cost function to derive hospital-specific measures of inefficiency. The cost function includes direct measures of illness severity, output quality, and patient outcomes to reduce the likelihood that the inefficiency estimates are capturing unmeasured differences in hospital outputs. Models are estimated using data from the AHA Annual Survey, Medicare Hospital Cost Reports, and MEDPAR. We explicitly test the assumption of output endogeneity and reject it in this application. We conclude that inefficiency accounts for 13.6 percent of total hospital costs. This estimate is robust with respect to model specification and approaches to pooling data across distinct groups of hospitals.     

Humeral head replacement for glenohumeral arthritis

From July 1977 through March of 1983, humeral head replacement was performed on 35 shoulders with osteoarthritis and 32 shoulders with rheumatoid arthritis and followed-up for an average of 9.3 years. Satisfactory pain relief was achieved in 44 (66%) and 52 of the shoulders (78%) were described by patients as being much better or better. Active elevation was improved from an average of 84 degrees to an average of 110 degrees with external rotation improving from 20 degrees to 44 degrees. Strength improvement also occurred. Only three complications developed, and these did not affect the final outcome. Because of moderate or severe pain, 12 shoulders (18%) required revision to total shoulder arthroplasty, and all patients were relieved of their pain. The result ratings were excellent in 10 shoulders, satisfactory in 23, and unsatisfactory in 34 (51%). With longer follow-up, a satisfactory level of pain relief may not continue for those patients with osteoarthritis and rheumatoid arthritis who have had humeral head replacement alone. Whereas this form of treatment should certainly be considered in those patients who have inadequate glenoid bone to support a glenoid implant and probably be considered in younger patients or patients who wish to remain more active, these latter patients must be fully appraised that the probability of continuing pain relief is less than has often been appreciated.     

Intrafamilial relations of cardiovascular disease risk factors in African-Americans: longitudinal results from DC SCAN

BACKGROUND: Few studies have examined intrafamilial patterns of cardiovascular disease (CVD) risk factors in African-American families or identified potential influences on these patterns. This study examines the effects of age and sex of child on correlations between siblings during childhood as well as between mothers and their offspring in African-American families at two points in time. METHODS: CVD risk factors were assessed in a sample of 267 pairs of African-American siblings and their mothers. One hundred nine of these families were selected for a second assessment of CVD risk factors approximately 28 months later. RESULTS: Older siblings had significantly greater correlations than younger siblings with mothers' low-density lipoproteins (r = 0.61 versus r = 0.43 for older and younger siblings, respectively), apolipoprotein A-I (r = 0. 46 versus r = 0.16), and lipoprotein (a) (r = 0.71 versus r = 0.34). Correlations between female siblings were significantly higher than between male siblings for total cholesterol (r = 0.74 versus r = 0. 18 for female versus male siblings), triglycerides (r = 0.56 versus r = 0.05), and apolipoprotein B (r = 0.72 versus r = 0.31); they were also higher between female siblings than between mixed-sex siblings for measures of adiposity (r = 0.46 versus r = 0.19) and total cholesterol (r = 0.74 versus r = 0.27). CONCLUSIONS: Significant intrafamilial correlations for African-American children were influenced by both age and sex of siblings, reflecting potential genetic and environmental influences. Assessing family patterns of CVD risk factors in high-risk populations may assist in the early identification of children who can benefit most from intervention.     

Antisense mapping KOR-1: evidence for multiple kappa analgesic mechanisms

In binding assays, both dynorphin B and alpha-neoendorphin are relatively selective for the kappa1b site, unlike U50,488H which has high affinity for both kappa1a and kappa1b sites. In vivo, U50,488H, dynorphin B and alpha-neoendorphin analgesia are reversed by the kappa1-selective antagonist, nor-binaltorphimine (norBNI). Antisense mapping the three exons of KOR-1 revealed that probes targeting all three exons blocked U50,488H analgesia, as expected. However, the selectivity profile of dynorphin B and alpha-neoendorphin analgesia towards the various antisense oligodeoxynucleotides differed markedly from U50,488H, implying a different receptor mechanism of action.