The Economics and Politics of Contracting out with the Private Sector: Evidence from the US Transit Industry

The paper studies contracting practices in the US transit industry. It employs the methods of transaction cost economics and public choice theory to develop an empirical model of bus contracting in the US transit industry. The empirical results shed light on why transit services in the US remain largely public, despite many attempts to introduce competition by contracting out services to the private sector. The results show that the decision by transit agencies to contract out with the private sector is constrained by the transaction costs of contracting and the institutional and subsidy arrangements that govern the transit industry in the US. Services that require idiosyncratic investments to provide large densities of passengers are less likely to be contracted out than those services that are provided using standard, small vehicles. Similarly, increases in federal subsidies and dedicated subsidies are found to discourage contracting out with the private sector. On the other hand, increases in state and local subsidies, other things being equal, encourage contracting. Agencies that have high labor costs –– indicating strong labor unions –– are less likely to contract out. In light of these findings, the paper concludes that piecemeal contracting out of services is not likely to increase the role of the private sector in the provision of public transit services. Structures of subsidies and federal arrangements creates intertwined incentives that discourage contracting by transit agencies, thus foiling the attempts to increase efficiencies by establishing competition for transit markets.Institute of Transport and Logistics Studies. Faculty of Economics and Business. The University of Sydne

Does supportive pamidronate treatment prevent or delay the first manifestation of bone metastases in breast cancer patients?

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Role of bone and kidney in tumor-induced hypercalcemia and its treatment with bisphosphonate and sodium chloride

The efficacy of intravenous aminohydroxypropylidene bisphosphonate as treatment for the hypercalcemia of malignancy was examined in a phase II multicenter study in 132 patients with a large variety of primary tumors. This provided an opportunity for an analysis of the separate influences of bone resorption and renal calcium handling on the genesis and maintenance of hypercalcemia. The results demonstrated that increased bone resorption is the major contributory factor and that inhibition with bisphosphonate normalizes the serum calcium concentration within five days in more than 90 percent of patients. Hypercalcemia is sustained by an inability of the kidney to deal efficiently with a chronically increased calcium load. This is influenced by the requirements of volume regulation in the presence of a sodium diuretic effect of hypercalcemia and is very sensitive to induced variations of sodium load. In addition, in a minority of patients, direct renal actions of tumor-derived humoral factors adversely reduce the ability to excrete calcium. For optimal treatment of tumor-induced hypercalcemia, bisphosphonate treatment should be combined with intravenous administration of saline solution

Population pharmacokinetics and pharmacodynamics of paclitaxel and carboplatin in ovarian cancer patients: A study by the European Organization for Research and Treatment of Cancer-Pharmacology and Molecular Mechanisms Group and New Drug Development Group

PURPOSE: Paclitaxel and carboplatin are frequently used in advanced ovarian cancer following cytoreductive surgery. Threshold models have been used to predict paclitaxel pharmacokinetic-pharmacodynamics, whereas the time above paclitaxel plasma concentration of 0.05 to 0.2 micromol/L (t(C > 0.05-0.2)) predicts neutropenia. The objective of this study was to build a population pharmacokinetic-pharmacodynamic model of paclitaxel/carboplatin in ovarian cancer patients. EXPERIMENTAL DESIGN: One hundred thirty-nine ovarian cancer patients received paclitaxel (175 mg/m(2)) over 3 h followed by carboplatin area under the concentration-time curve 5 mg/mL*min over 30 min. Plasma concentration-time data were measured, and data were processed using nonlinear mixed-effect modeling. Semiphysiologic models with linear or sigmoidal maximum response and threshold models were adapted to the data. RESULTS: One hundred five patients had complete pharmacokinetic and toxicity data. In 34 patients with measurable disease, objective response rate was 76%. Neutrophil and thrombocyte counts were adequately described by an inhibitory linear response model. Paclitaxel t(C > 0.05) was significantly higher in patients with a complete (91.8 h) or partial (76.3 h) response compared with patients with progressive disease (31.5 h; P = 0.02 and 0.05, respectively). Patients with paclitaxel t(C > 0.05) >61.4 h (mean value) had a longer time to disease progression compared with patients with paclitaxel t(C > 0.05) > 61.4 h (89.0 versus 61.9 weeks; P = 0.05). Paclitaxel t(C < 0.05) was a good predictor for severe neutropenia (P = 0.01), whereas carboplatin exposure (C(max) and area under the concentration-time curve) was the best predictor for thrombocytopenia (P > 10(-4)). CONCLUSIONS: In this group of patients, paclitaxel t(C > 0.05) is a good predictive marker for severe neutropenia and clinical outcome, whereas carboplatin exposure is a good predictive marker for thrombocytopenia

Population pharmacokinetics and pharmacodynamics of paclitaxel and carboplatin in ovarian cancer patients: A study by the European Organization for Research and Treatment of Cancer-Pharmacology and Molecular Mechanisms Group and New Drug Development Group

PURPOSE: Paclitaxel and carboplatin are frequently used in advanced ovarian cancer following cytoreductive surgery. Threshold models have been used to predict paclitaxel pharmacokinetic-pharmacodynamics, whereas the time above paclitaxel plasma concentration of 0.05 to 0.2 micromol/L (t(C > 0.05-0.2)) predicts neutropenia. The objective of this study was to build a population pharmacokinetic-pharmacodynamic model of paclitaxel/carboplatin in ovarian cancer patients. EXPERIMENTAL DESIGN: One hundred thirty-nine ovarian cancer patients received paclitaxel (175 mg/m(2)) over 3 h followed by carboplatin area under the concentration-time curve 5 mg/mL*min over 30 min. Plasma concentration-time data were measured, and data were processed using nonlinear mixed-effect modeling. Semiphysiologic models with linear or sigmoidal maximum response and threshold models were adapted to the data. RESULTS: One hundred five patients had complete pharmacokinetic and toxicity data. In 34 patients with measurable disease, objective response rate was 76%. Neutrophil and thrombocyte counts were adequately described by an inhibitory linear response model. Paclitaxel t(C > 0.05) was significantly higher in patients with a complete (91.8 h) or partial (76.3 h) response compared with patients with progressive disease (31.5 h; P = 0.02 and 0.05, respectively). Patients with paclitaxel t(C > 0.05) >61.4 h (mean value) had a longer time to disease progression compared with patients with paclitaxel t(C > 0.05) > 61.4 h (89.0 versus 61.9 weeks; P = 0.05). Paclitaxel t(C < 0.05) was a good predictor for severe neutropenia (P = 0.01), whereas carboplatin exposure (C(max) and area under the concentration-time curve) was the best predictor for thrombocytopenia (P > 10(-4)). CONCLUSIONS: In this group of patients, paclitaxel t(C > 0.05) is a good predictive marker for severe neutropenia and clinical outcome, whereas carboplatin exposure is a good predictive marker for thrombocytopenia