No abstract

The Health Care Financing Administration (HCFA) publishes hospital mortality rates each year. We undertook a study to identify characteristics of hospitals associated with variations in these rates. To do so, we obtained data on 3100 hospitals from the 1986 HCFA mortality study and the American Hospital Association's 1986 annual survey of hospitals. The mortality rates were adjusted for each hospital's case mix and other characteristics of its patients. The mortality rate for all hospitalizations was 116 per 1000 patients. Adjusted mortality rates were significantly higher for for-profit hospitals (121 per 1000) and public hospitals (120 per 1000) than for private not-for-profit hospitals (114 per 1000; P less than 0.0001 for both comparisons). Osteopathic hospitals also had an adjusted mortality rate that was significantly higher than average (129 per 1000; P less than 0.0001). Private teaching hospitals had a significantly lower adjusted mortality rate (108 per 1000) than private nonteaching hospitals (116 per 1000; P less than 0.0001). Adjusted mortality rates were also compared for hospitals in the upper and lower fourths of the sample in terms of certain hospital characteristics. The mortality rates were 112 and 121 per 1000 for the hospitals in the upper and lower fourths, respectively, in terms of the percentage of physicians who were board-certified specialists (P less than 0.0001), 112 and 120 per 1000 for occupancy rate (P less than 0.0001), 113 and 120 per 1000 for payroll expenses per hospital bed (P less than 0.0001), and 113 and 119 per 1000 for the percentage of nurses who were registered (P less than 0.0001).

SynopsisThe heats of the conformational transitions of poly(A + U) and poly(A + 2U) were determined in a twin-cell differential thermal analysis microcalorimeter capable of measuring heat effects of 25-35 mcal. in reactions of this type, with a precision of about 37,. The dependence of these heats on the concentration of Na+ and K+ was studied and was found to be interpretable with fair success by a simple phenomenological argument which employs the concept of binding of counterions to polyelectrolytes.

The relationship between the presence of antibody to hepatitis B core antigen (anti-HBc) in donor blood and the development of hepatitis in recipients of that blood was studied in 6293 blood donors and 481 recipients who were followed for 6 to 9 months after transfusion. Of 193 recipients of at least 1 unit of blood positive for anti-HBc, 23 (11.9%) developed non-A, non-B hepatitis compared with 12 (4.2%) of 288 recipients of only anti-HBc-negative blood (p less than 0.001). Donor anti-HBc status was not significantly associated with the development of hepatitis B in the recipient and was negatively associated with the development of cytomegalovirus hepatitis. The relationship of donor anti-HBc status and the development of non-A, non-B hepatitis in the recipient was independent of transfusion volume and elevated donor transaminase level. Although 88% of anti-HBc-positive blood units were not associated with recipient non-A, non-B hepatitis, calculation of maximal corrected efficacy predicted that exclusion of anti-HBc-positive donors might have prevented 43% of the cases of non-A, non-B hepatitis with a donor loss of 4%. Because of the serious chronic consequences of non-A, non-B hepatitis, surrogate tests for non-A, non-B virus carriers must be seriously considered.