Contracting plays a significant role in U.S. public transit provision, but there is a gap between the majority of quantitative studies that report significant cost savings from contracting and the few qualitative studies that consider the political nature of an agency's decision about contracting. To fill this gap, the authors systematically examined agency decisions about contracting, by interviewing managers and directors at 13 California transit agencies. In interviews with agencies of various sizes and blends of contracted and in-house services, it was found that agencies have responded differently to fiscal pressures and to contracting as a provision strategy. Some have readily adopted contracting to provide all services, while others have used different strategies, such as part-time labor and varying wage scales, to enhance their cost-efficiency. Those responses are a result not just of economic analysis but also of the agency's institutional environment, relationship with its labor union, and the political and economic contexts in which it operates. This study broadens the current understanding of contracting as practiced by transit agencies today–-in particular, why agencies choose to contract or not and how agencies have used both contracting and other means to respond to financial pressure. The findings reemphasize that it is important for an individual transit agency to assess carefully its service lines and various measures of increasing cost-efficiency, and to maintain a cooperative relationship with its unions to determine an appropriate level of contracting for its own operating environment.

Lipoprotein lipase (LPL) is a key regulator of triglyceride clearance. Its coordinated regulation during feeding and fasting is critical for maintaining lipid homeostasis and energy supply. Angiopoietin-like (Angptl)3 and Angptl4 are secreted proteins that have been demonstrated to regulate triglyceride metabolism by inhibiting LPL. We have taken a targeted genetic approach to generate Angptl4- and Angptl3-deficient mice as well as transgenic mice overexpressing human Angptl4 in the liver. The Angptl4 transgenic mice displayed elevated plasma triglycerides and reduced postheparin plasma (PHP) LPL activity. A purified recombinant Angptl4 protein inhibited mouse LPL and recombinant human LPL activity in vitro. In contrast to the transgenic mice, Angptl4-deficient mice displayed hypotriglyceridemia and increased PHP LPL activity, with greater effects in the fasted compared with the fed state. Angptl3-deficient mice also displayed hypotriglyceridemia with elevated PHP LPL activity, but these mice showed a greater effect in the fed state. Mice deficient in both Angptl proteins showed an additive effect on plasma triglycerides and did not survive past 2 months of age. Our results show that Angptl3 and Angptl4 function to regulate circulating triglyceride levels during different nutritional states and therefore play a role in lipid metabolism during feeding/fasting through differential inhibition of LPL.

BACKGROUND:Standard rat cecal ligation and puncture (CLP) results in only transient hyperglycemia, making an examination of the effects of glucoregulatory agents, such as insulin, on the morbidity and mortality of CLP problematic. Accordingly, we sought to develop a model of rat CLP with prolonged hyperglycemia through continuous infusion of total parenteral nutrition (TPN) post CLP. MATERIALS AND METHODS:Polyethylene catheters were implanted into the femoral vein of female Sprague Dawley rats (245-265 g) which were subsequently subjected to CLP. TPN was initiated at different intervals following CLP, and mortality, bacteremia, blood glucose, hormonal, and inflammatory responses were monitored. RESULTS:Without TPN, CLP resulted in significantly lower blood glucose at 22 h post CLP. In contrast, CLP rats receiving TPN exhibited significant prolonged hyperglycemia that was responsive to insulin treatment. Mortality and hyperglycemia tended to increase with puncture size in CLP TPN rats, with early initiation of TPN leading to poorer outcome. There were time-dependent differences in bacteremia and mortality based on time of TPN initiation. Levels of insulin, leptin, and glucagon were significantly elevated in CLP TPN rats, as were many inflammatory markers. Organ damage was evident as early as 12 h post CLP and blood cell kinetics indicated significantly depressed neutrophil and lymphocyte counts. CONCLUSIONS:Our results indicate that addition of TPN to CLP provides a clinically relevant animal model of critical illness with associated hyperglycemia that may provide utility for the testing of glucoregulatory and other therapeutic modalities.