Privatizing maternal and child health services in Texas: reinventing Title V programs.

In November 1994, the Texas Department of Health embarked upon a major initiative to "reinvent" maternal and child health services funded through the Title V Maternal and Child Health Block Grant and related state general revenue. This article describes the rationale, planning process, and implementation issues associated with the initiative to redefine the fundamental roles and priorities of the department and traditional public health entities in the delivery of maternal and child health services.

Induction of invasive and degradative phenotype in normal synovial fibroblasts exposed to synovial fluid from patients with juvenile rheumatoid arthritis: role of mononuclear cell population.

OBJECTIVE: To investigate the effect of synovial fluid (SF) from patients with juvenile rheumatoid arthritis (JRA) on proliferation and induction of degradative and invasive phenotype in normal synovial fibroblasts, and to elucidate the contribution of SF cells to this activity. METHODS: SF and/or conditioned medium (CM) from SF cells were evaluated for their ability to (1) stimulate a proliferative response, (2) induce the "activated phenotype" capable of invading cartilage matrix, and (3) promote the release of key matrix metalloproteinases (MMP) in normal synovial fibroblasts. RESULTS: Proliferation of normal synovial fibroblasts exposed to SF or CM from SF cells of patients with JRA was up to 3 times greater than untreated controls. Concomitant with induction of an activated phenotype in the treated synovial fibroblasts, the activated form exhibited up to 250% invasiveness of cartilage matrix compared to untreated synovial fibroblasts (100%), in addition to releasing increased MMP activity, not normally associated with these quiescent cells. This induction was not solely due to tumor necrosis factor-alpha, transforming growth factor-beta, interleukin 1beta (IL-1beta), and IL-6, as SF and/or CM depleted of these cytokines sustained about 40% of their invasive and inducing ability. We observed that the mononuclear cell (MNC) population that infiltrated into the joint cavity secretes this "inducing activity," which can be maintained in culture up to several weeks. CONCLUSION: Our data suggest that the cellular component of SF releases soluble factor(s) that directly or indirectly contribute to (a) proliferation of synovial fibroblasts, and (b) production and release of extracellular MMP by synovial fibroblasts, thereby inducing a degradative and invasive phenotype culminating in cartilage and bone destruction.

Rapid movement kinematic and electromyographic control characteristics in males and females.

Maximally fast, self-terminated elbow flexion movements were performed by 10 male and 10 female college-aged subjects to assess potential gender-related differences in kinematics and the triphasic electromyographic (EMG) pattern. The subjects were instructed to move their forearms as fast as possible through 90 degrees of elbow flexion range of motion and stop as sharply as possible at the terminal point. An electromagnet, set to 0, 40, and 70% of each subject's maximal isometric torque, provided resistance to movement initiation and resulted in quick release movements. Surface EMG was collected from the biceps b. and triceps b. muscles. Results indicated that the males had faster movements and accelerations under all conditions. EMG records indicated that the males had faster rates of EMG rise, particularly in the triceps b., and more tightly coupled reciprocal activation. The quick release afforded faster accelerations for both groups, yet only the males moved faster throughout the full range of motion. Following the quick release, the males differed from the females by increasing the triceps b. EMG amplitude. Hence, the males were able to shorten movement time in quick release movements by increasing triceps b. activation and, thus, braking ability. These results suggest that the females were more neurally constrained than the males with respect to rapid EMG activation of the triceps b., resulting in limits in the braking process.