Search

A novel CMOS transmit/receive (T/R) switch suitable for ultra-low-voltage operations is presented in this paper. Due to the use of resonators in the receiving and transmitting paths, enhanced performance in terms of insertion losses and isolation can be achieved. In addition, the forward-body-bias and body-floating techniques are also introduced to minimize the on-resistance of the MOSFETs at a reduced bias voltage. Using a standard 0.18-mum CMOS process, a 5.2-GHz asymmetric T/R switch based on the proposed architecture is implemented. With a supply voltage of 0.6 V, the fabricated circuit exhibits 1.56-dB insertion loss, 17-dB isolation, and 11.2-dBm in the receiving mode while the measured results in the transmitting mode are 2.02 dB, 31 dB, and 29.6 dBm, respectively.

It is generally accepted that bacterial endotoxin (lipopolysaccharide, LPS) acts via endogenous mediators leading to endotoxicity. Among these endogenous mediators, tumor necrosis factor-alpha (TNF-alpha) seems to induce all characteristics for endotoxemia. Inhibition of TNF-(alpha production by cAMP-elevating agents has been well documented. Terbutaline (an agonist of beta2-adrenoceptor) and dobutamine (an agonist of beta1-adrenoceptor), both are able to increase intracellular cAMP via activation of adenylate cyclase, were examined in the anesthetized rat with endotoxemia. Terbutaline or dobutamine was administered to the rat at 30 min after LPS injection. Hemodynamic changes and plasma TNF-alpha and nitrate (the end product of nitric oxide [NO]) levels as well as superoxide anion (O2*-) production in the aorta were examined in this study. Results showed that terbutaline, but not dobutamine, improved the circulatory failure (e.g. hypotension and vascular hyporeactivity) in rats with endotoxemia. In addition, both terbutaline and dobutamine reduced the plasma TNF-alpha level, but only terbutaline attenuated the aortic O2*- production in these endotoxemic rats. The beneficial effect of terbutaline in endotoxemic animals was associated with a reduction in plasma TNF-alpha and aortic O2*-, but not in plasma NO.

Despite the fact that septic shock is characterized by a decrease in systemic vascular resistance, the main cause of death is due to multiple organ failure. The organ dysfunction is usually attributed to cell death caused by overproduction of free radicals derived from inflammation. In the host infected by endotoxin (lipopolysaccharide, LPS), the expression and release of proinflammatory tumor necrosis factor-alpha (TNF-alpha) rapidly increases, and the formation of free radicals (e.g., superoxide anion [O2*-] and nitric oxide [NO*] in the present study) are inevitably overproduced. In this study, we present evidence that overall treatment of LPS rats with terbutaline, a beta2-adrenoceptor agonist, attenuates the delayed hypotension and ameliorates the tachycardia. Overproduction of TNF-alpha and NO* (produced by inducible NO synthase [iNOS] examined by Western blot analysis in the lung and the liver) is inhibited by treatment of LPS rats with terbutaline. In addition, treatment of endotoxemic rats with terbutaline also reduces the O2*- levels in the lung and the liver. Terbutaline also improves the liver (assessed by aspartate aminotransferase, alanine aminotransferase, total bilirubin, and albumin/globulin) and kidney (assessed by creatinine and uric acid) dysfunction induced by endotoxin. These findings suggest that the amelioration of circulatory failure and organs injury by terbutaline is associated with its suppression in TNF-alpha, O2*- and NO (via iNOS) production in animals with endotoxic shock.