Universities as resources to state health agencies.

In a survey of the 50 State health agencies in the spring of 1992, officials were asked about their manpower and research needs in the specific areas of administration, behavioral and social science, education and information, environmental health, environmental protection, epidemiology, laboratory, law, occupational health, policy and planning, and statistics. In all, 40 agencies (80 percent) responded. Indepth telephone interviews to determine whether universities and schools and graduate programs in public health filled these needs completed the data collection process. Agency officials indicated that their resources were least adequate in environmental protection, behavioral and social science, and occupational health. They did not feel their research needs were being met. There was a general feeling that universities and schools and programs in public health have different agendas than State agencies and that practical solutions to the shortage of research resources are not forthcoming from these sources. Suggestions are made as to what can be done to improve relationships between those who train public health personnel and those who employ them.     

CD4-specific monoclonal antibody can prolong cardiac allograft survival without T-cell depletion

Current immunosuppressive regimens for clinical transplantation are immunologically non-specific, are associated with acute and chronic toxic side-effects [1] and are unable to prevent chronic graft loss in a significant proportion of patients. Additionally, new and increasingly powerful drugs are being introduced to induce non-specific immunosuppression, and therefore this is likely to be followed by an increase in related complications such as the induction of cancers. Hence, there is a need for an alternative approach. It has been shown that long-term survival of murine cardiac grafts can be induced by the monoclonal antibody YIS 191 that depletes CD4 ⁺T cells in vivo [2]. In this study, we have investigated the ability of a non-depleting antibody to produce better graft survival.     

An Interdisciplinary Clinical Advancement Program Within a Patient-Centered Care Model

Restructuring in health care does not have to compromise the pursuit of clinical excellence and quality patient care. The clinical advancement program (CAP) at the Hospital for Special Care is a newly developed multidisciplinary reward and recognition program for clinical staff. The program is integrated into the hospital's structure of service line management and, unlike traditional advancement programs, is open to all levels of care providers: professional personnel, technical staff, and aides. This article describes the basic features of the CAP model and how it was developed by a multidisciplinary task force.     

Inhibition of mediator release in systemic mastocytosis is associated with reversal of bone changes

A 59-year-old male presented with systemic mastocytosis with extensive skeletal involvement resulting in vertebral compression fractures and bone pain. Histomorphometric analysis of bone revealed increased mast cells, elevated static parameters of bone resorption, and low bone formation. Serum calcium, phosphorus, and alkaline phosphatase were normal; however, serum 1,25-dihydroxyvitamin D3 and osteocalcin levels were low. Histamine levels in plasma and urine were elevated. Following therapy with ketotifen, the patient had resolution of bone pain along with decreased flushing and pruritus. Elevated plasma and urine histamine levels normalized, as did 1,25-dihydroxyvitamin D3 and osteocalcin levels. Indices of low bone formation improved on therapy. Eroded surfaces improved but remained elevated. This case is the first demonstration that bone symptoms and histomorphometric change in systemic mastocytosis are reversed with inhibition of mast cell degranulation. The role of mast cells and their products in bone metabolism is poorly understood, but the therapy of bone disease in systemic mastocytosis should include inhibition of the release of mast cell products along with the use of histamine antagonist.