Congressional acquiescence to presidentialism in the US ‘War on Terror’

Congressional dominance theory holds that not only can the US Congress control the executive, it does. The terrorist attacks on New York and Washington on 11 September 2001 and the Bush administration's ensuing global 'war on terror' suggest a different result. Bush's response to 9/11 signalled not only new directions in US foreign and domestic policy but a new stage in the aggrandisement of presidential power in the United States and a further step in the marginalisation of the Congress. Informed by a constitutional doctrine unknown to the framers of the US Constitution, the Bush administration pursued a presidentialist or 'ultra-separationist' governing strategy that was disrespectful to the legislature's intended role in the separated system. Using its unilateral powers, in public and in secret, claiming 'inherent' authority from the Constitution, and exploiting the public's fear of a further terrorist attack and of endangering the lives of US troops abroad, the administration skilfully drove its legislation through the Congress. Occasionally, the Congress was able to extract concessions - notably in the immediate aftermath of 9/11, when partisan control of the government was split - but more typically, for most of the period, the Congress acquiesced to administration demands, albeit with the consolation of minor concessions. The administration not only dominated the lawmaking process, it also cowed legislators into legitimating often highly controversial (and sometimes illegal) administration-determined definitions of counter-terrorism and national security policy. Certainly, the Congress undertook a considerable amount of oversight during the period of the 'war on terror'; lawmakers also complained. But the effects on policy were marginal. This finding held true for periods of Democratic as well as Republican majorities.

A new bulk-driven input stage design for sub 1-volt CMOS op-amps

This paper presents a new design approach for a rail-to-rail bulk-driven input stage using a standard single-well (n-well in this paper) CMOS technology. This input stage can provide nearly constant transconductance and constant slew rate over the entire input common-mode voltage, operating with a wide supply voltage ranging from sub 1-volt (V/sub T0/+ 3V/sub DSsat/) to the maximum allowed for the CMOS process, as well as preventing latch-up.

Protein deiminases: new players in the developmentally regulated loss of neural regenerative ability

Spinal cord regenerative ability is lost with development, but the mechanisms underlying this loss are still poorly understood. In chick embryos, effective regeneration does not occur after E13, when spinal cord injury induces extensive apoptotic response and tissue damage. As initial experiments showed that treatment with a calcium chelator after spinal cord injury reduced apoptosis and cavitation, we hypothesized that developmentally regulated mediators of calcium-dependent processes in secondary injury response may contribute to loss of regenerative ability. To this purpose we screened for such changes in chick spinal cords at stages of development permissive (E11) and non-permissive (E15) for regeneration. Among the developmentally regulated calcium-dependent proteins identified was PAD3, a member of the peptidylarginine deiminase (PAD) enzyme family that converts protein arginine residues to citrulline, a process known as deimination or citrullination. This post-translational modification has not been previously associated with response to injury. Following injury, PAD3 up-regulation was greater in spinal cords injured at E15 than at E11. Consistent with these differences in gene expression, deimination was more extensive at the non-regenerating stage, E15, both in the gray and white matter. As deimination paralleled the extent of apoptosis, we investigated the effect of blocking PAD activity on cell death and deiminated-histone 3, one of the PAD targets we identified by mass-spectrometry analysis of spinal cord deiminated proteins. Treatment with the PAD inhibitor, Cl-amidine, reduced the abundance of deiminated-histone 3, consistent with inhibition of PAD activity, and significantly reduced apoptosis and tissue loss following injury at E15. Altogether, our findings identify PADs and deimination as developmentally regulated modulators of secondary injury response, and suggest that PADs might be valuable therapeutic targets for spinal cord injury.