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New quick-response and high-efficiency control of an induction motor, which is quite different from that of the field-oriented control is proposed. The most obvious differences between the two are as follows. 1) The proposed scheme is based on limit cycle control of both flux and torque using optimum PWM output voltage; a switching table is employed for selecting the optimum inverter output voltage vectors so as to attain as fast a torque response, as low an inverter switching frequency, and as low harmonic losses as possible.2) The efficiency optimization in the steady-state operation is also considered; it can be achieved by controlling the amplitude of the flux in accordance with the torque command. To verify the feasibility of this scheme, experimentation, simulation, and comparison with field-oriented control are carried out. The results prove the excellent characteristics for torque response and efficiency, which confirm the validity of this control scheme.

We investigated the functions of adiponectin, an adipocyte-specific secretory protein and a new member of the family of soluble defense collagens, in hematopoiesis and immune responses. Adiponectin suppressed colony formation from colony-forming units (CFU)—granulocyte-macrophage, CFU-macrophage, and CFU-granulocyte, whereas it had no effect on that of burst-forming units—erythroid or mixed erythroid-myeloid CFU. In addition, adiponectin inhibited proliferation of 4 of 9 myeloid cell lines but did not suppress proliferation of erythroid or lymphoid cell lines except for one cell line. These results suggest that adiponectin predominantly inhibits proliferation of myelomonocytic lineage cells. At least one mechanism of the growth inhibition is induction of apoptosis because treatment of acute myelomonocytic leukemia lines with adiponectin induced the appearance of subdiploid peaks and oligonucleosomal DNA fragmentation. Aside from inhibiting growth of myelomonocytic progenitors, adiponectin suppressed mature macrophage functions. Treatment of cultured macrophages with adiponectin significantly inhibited their phagocytic activity and their lipopolysaccharide-induced production of tumor necrosis factor α. Suppression of phagocytosis by adiponectin is mediated by one of the complement C1q receptors, C1qRp, because this function was completely abrogated by the addition of an anti-C1qRp monoclonal antibody. These observations suggest that adiponectin is an important negative regulator in hematopoiesis and immune systems and raise the possibility that it may be involved in ending inflammatory responses through its inhibitory functions.

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