Abstract: The present application generally relates to the discovery that glycogen synthase kinase 3 (GSK-3) is an upstream signalling molecule that controls PD-1 transcription and Tbet expression by immune cells and in particular T-cells. Based on this discovery, and in view of the known immunosuppressive effect of PD-1 on immunity and the promoting effect of Tbet on T cell immunity, the present invention relates to the use of GSK-3 inhibitors to promote immunity, including cytotoxic T cell immunity in subjects in need thereof, especially subjects with chronic conditions wherein inhibiting PD-1 expression and/or blockade or Tbet up-regulation is therapeutically desirable such as cancer and infectious conditions. Further, based on this discovery the present invention relates to the use of compounds which promote GSK-3 expression or activity to suppress immunity, especially aberrant T cell immunity in subjects in need thereof, e.g.

Abstract: The invention concerns the identification of a pathway where the co-receptor CD28 inactivates glycogen synthase 3 (GSK-3) and where a reagent that inhibits GSK-3 can enhance, or substitute for CD28-dependent T-cell mediated immune responses. Altered T-cell responses are applied to increased proliferation, cytokine production and in the generation of increased cytolytic T-cell responses (CTLs) in the context of infection by virus', bacterial, fungi or prions. For example, the use of GSK-3 inhibitor SB415286 preferentially cooperated with CD28 costimulation to increase interleukin 2 (IL-2) transcription, and to provide CD28-replacement signals leading to increased IL-2 transcription. Similarly, inhibitors SB415286 and lithium chloride increased the CD28-dependent generation of cytolytic T-cell responses (CTLs) against a virally or baterially infected cells.

Abstract: A rotor position transducer for an electronically commutated electric motor has a vane mounted to rotate with the rotor and a pair of sensors, according to one embodiment. One sensor has an output coincident with positions of zero torque. The other sensor produces signals slightly in advance. Overlapping portions of the signals denote regions of different levels of torque. The second sensor output can also be used in high-speed, single-pulse control of the motor. Method embodiments and other apparatus embodiments are also disclosed.

Abstract: A single-phase variable reluctance motor is disclosed. The motor includes a stator having a pair of projecting poles defining a principal axis and a rotor mounted on a rotatable shaft co-axial with the principal axis of the stator. The stator may have inwardly extending poles that terminate in a central bore and the rotor may be rotatably disposed in the central bore. In such an embodiment, the stator poles are arranged generally diametrically opposed to one another. The rotor is mounted on a shaft and has a pair of poles generally diametrically opposed from each other. The stator and rotor may be formed from laminations of a ferromagnetic material. Energizing coils are wound around one or more of the stator poles. When energized, the energizing coil(s) impart a torque on the rotor causing it to rotate. One or more permanent magnets are inserted into the winding(s) forming the energizing coil(s) to park the rotor in a preferred starting position when the motor is turned off.

Abstract: This invention concerns alteration of the interaction of PTKs and T-cell receptors. We have found that PTKs and T-cell receptors are complexed within the T-cell and the formation of this complex dictates the susceptibility of the T-cell to activation and to infection by viruses such as HIV. The nature of the interaction between the kinase and the T-cell receptor in a human is also related to the potential for cancer cell formation in that human, and to susceptibility to an autoimmune disease. Modified p56.sup.lck and transfected mammalian cells expressing the same are disclosed.

Abstract: This invention concerns alteration of the interaction of PTKs and T-cell receptors. We have found that PTKs and T-cell receptors are complexed within the T-cell and the formation of this complex dictates the susceptibility of the T-cell to activation and to infection by viruses such as HIV. The nature of the interaction between the kinase and the T-cell receptor in a human is also related to the potential for cancer cell formation in that human, and to susceptibility to an autoimmune disease. Modified CD4 and CD8 T cell receptors and transfected mammalian cells expressing the same are disclosed.

Abstract: An essentially purified antigen comprising a protein present in the T-cells of Aotus trivirgatus having molecular weights of 140 KD and 105 KD under reducing conditions and 120 KD and 90 KD under non-reducing conditions, antibodies against this antigen, and a method of using these antibodies to activate T-cells. The antibodies are able to induce T-cell activation in synergy with phorbol myristate acetate alone and with antibody against the T 11.sub.3 epitope of T 11 (CD.sub.2) antigen alone.