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This paper proposes a robust model for the accurate behavioral modeling and digital predistortion (DPD) of wideband radio-frequency power amplifiers (PAs). It is constructed using a complexity-reduced generalized memory polynomial (MP) (GMP) (CR-GMP) connected with a nonlinear memory effect (NME) subblock in parallel. The CR-GMP is a complexity-reduced but accuracy-degraded version of the conventional GMP, and its performance is augmented by the extra NME subblock. Hence, the proposed model is termed as augmented CR-GMP (ACR-GMP). The resultant ACR-GMP model can achieve comparable performance as the GMP model, but with much fewer coefficients and lower complexity. Its performance is experimentally assessed both in forward modeling and DPD linearization. Comparisons are conducted between the ACR-GMP model and some state-of-the-art models, such as the MP, the PLUME, and the GMP. Experimental results have been given for a 1.9-GHz 35-W peak-power GaN Class-AB PA driven by two signal scenarios: a 15-MHz bandwidth long-term-evolution signal and a 20-MHz bandwidth widebandcode-division-multiple-access 1001 signal (with the middle two carriers OFF). All the results show that the ACR-GMP model outperforms both the MP and the PLUME models in terms of performances and the GMP model in terms of complexity (at comparable performances).Index Terms-Behavioral modeling, digital predistortion (DPD), generalized memory polynomial (MP) (GMP), memory effect, MP, power amplifiers (PAs).

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Nonsteroidal antiinflammatory drugs (NSAIDs) are recognized for inhibiting growth of colon tumors in animal models, and for reducing the risk of colon cancer in humans. The mechanisms involved have not been established, but are thought to be related to reduced prostaglandin biosynthesis. The present study investigates the effect of COX-inhibiting and non-COX-inhibiting enantiomers of flurbiprofen on rat colonocyte proliferation. Intestinal ulceration was used as a surrogate indicator of COX inhibition. Sprague Dawley rats were treated orally with 6.3 mg/kg of R- or s-flurbiprofen or vehicle. Colonocyte labeling index and small bowel ulcer index were measured. R-flurbiprofen and S-flurbiprofen significantly reduced colonocyte labeling index, by 34% and 23% respectively, compared with vehicle. R-flurbiprofen caused minimal ulcer formation (4.48 mm2) compared with S-flurbiprofen (94.4 mm2). These findings suggest that R-flurbiprofen-mediated control of colonocyte proliferation is independent of prostaglandin biosynthesis.

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In human neutrophils, alkaline phosphatase (AlkPase), a low-affinity receptor for IgG (FcRIIIB), and complement decay accelerating factor (DAF) are glycosyl-phosphatidylinositol (GPI)-anchored proteins. Varying greatly in biological function these three integral membrane proteins exhibit regulated cell surface expression in neutrophils. Defined by their common membrane-linkage motif, AlkPase, FcRIIIB, and DAF can be released from the lipid bilayer by the action of phosphatidylinositol-specific phospholipase C and are relatively resistant to low temperature extraction with Triton X-100 (TX-100). In this study we show that neutrophil AlkPase, FcRIII, and DAF display differential extractibility; they are relatively insensitive to TX-100 solubilization at 4 degrees C, but are readily extracted with TX-100 at 37 degrees C or by the detergent octyl glucoside at 4 degrees C. The differential extractibility of these GPI-anchored proteins is the same in unstimulated cells, where these proteins exist primarily in an intracellular pool, and stimulated cells, where they are expressed principally at the cell surface. However, no differential extraction effect is observed with two neutrophil transmembrane proteins, complement receptor 1 (CD35, CR1) and MHC Class I in either stimulated or unstimulated cells.