Continuous phase quadrature phase shift keyed signaling techniquewith coding

A continuous phase quadrature phase shift keyed (CPQPSK) modulation technique is presented. This method utilizes a conventional QPSK modulator and a phase trajectory converter to approximate M=4, h=1/4 continuous phase signal and allows low cost, low complexity, and high rate (>1 Gbit/s) CPM modem implementation for bandwidth efficient transmission through nonlinear satellite channels. Using a communications analysis computer program it has been found that CPQPSK has 99 percent out-of-band power of 0.8R (MSK has 99 percent out-of-band power of 1.2 R where R is defined as bit rate), continuous phase trajectories, and nearly constant envelope amplitude. Simulation of realistic hardware designs indicate that the CPQPSK will require an Eb/No of 14 dB to achieve a bit error rate (BER) of 10^-6. Forward error correcting techniques using block codes with an overhead of 10 percent indicate that the Eb/No requirements can be reduced to 11.2 dB for 10^-6 BER     

Phase I trial of inhaled natural interleukin 2 for treatment of pulmonary malignancy: toxicity, pharmacokinetics, and biological effects

Safety, local and systemic immunomodulation, and tumor response to treatment with aerosolized natural interleukin 2 (nIL-2) applied five times a day were studied in a Phase I trial in 16 patients with pulmonary malignancies refractory to conventional therapy. The toxicity of inhaled nIL-2 was different from that observed after systemic administration. Reversible airway irritation causing a nonproductive cough represented the dose-limiting toxicity. Mild to moderate reduction of the vital capacity and forced expiratory volume (FEV1) with minor effects on relative FEV1, peak expiratory flow, airway resistance, and PaO2 was experienced by individual patients. In 14 patients suffering from pulmonary metastases due to renal cell cancer, one durable complete response, one partial response, and one mixed response were observed. Inhalation of nIL-2 aerosol resulted in a dose-dependent expansion of pulmonary immunocompetent cells in bronchoalveolar lavage fluid. Posttreatment bronchoalveolar lavage showed an activated lymphocyte phenotype with increased HLA-DR expression. The only systemic biological effect detectable in peripheral blood was a marked increase of soluble interleukin 2 receptor serum levels. We conclude that treatment with aerosolized nIL-2 is an effective means for site-specific immunomodulation and deserves further investigation for the treatment of malignant and inflammatory lung disease.     

Mass transfer across wind-sheared interfaces

A predictive analogy of turbulent mass transfer across wavy, sheared air-water interface, in deep water bodies is proposed. The theory is based on the formulation of a theoretical eddy diffusivity profile in the surface region, and it applies to the non-breaking wave regime. The predictions for a water-side friction velocity range of 0.5–6 cm/s are in excellent agreement with laboratory data from wind-wave facilities with an average error of 15.4%.     

Plasminogen activator inhibitor-1 secretion of endothelial cells increases fibrinolytic resistance of an in vitro fibrin clot: evidence for a key role of endothelial cells in thrombolytic resistance

Time-dependent thrombolytic resistance is a critical problem in thrombolytic therapy for acute myocardial infarction. Platelets have been regarded as the main source of plasminogen activator inhibitor-1 (PAI-1) found in occlusive platelet-rich clots. However, endothelial cells are also known to influence the fibrinolytic capacity of blood vessels, but their ability to actively mediate time-dependent thrombolytic resistance has not been fully established. We will show that, in vitro, tumor necrosis factor-alpha-stimulated endothelial cells secrete large amounts of PAI-1 over a period of hours, which then binds to fibrin and protects the clot from tissue plasminogen activator-induced fibrinolysis. In vivo, endothelial cells covering atherosclerotic plaques are influenced by cytokines synthesized by plaque cells. Therefore, we propose that continuous activation of endothelial cells in atherosclerotic blood vessels, followed by elevated PAI-1 secretion and storage of active PAI-1 in the fibrin matrix, leads to clot stabilization. This scenario makes endothelial cells a major factor in time-dependent thrombolytic resistance.