Felon Disenfrachisement Laws: Partisan Politics in the Legislatures

This examination of the institutional changes to state legislatures, synthesized with an analysis of the handling of felon disenfranchisement laws by state legislatures, presents a troubling realization about the law today: in the twenty-first century, partisan politics moderates decisions about even the most basic and fundamental principles of democracy. This Note suggests that because state legislators follow their party leadership and position, a state\u27s traditional treatment of racial minorities, geographic location, and even ideology are not the strongest indicators of a state\u27s disenfranchisement laws. Rather, partisan politics drives changes to the state laws governing felon voter eligibility

RACE AGAINST THE MACHINE: AN ARGUMENT FOR THE STANDARDIZATION OF VOTING TECHNOLOGY

In this article/note, I examine a lingering question from the court cases arising out of the 2000 election: Does Bush v. Gore and the relevant equal protection case law open the door for a legal challenge to a state’s use of different voting machines/technologies and how do racial disparities in machine error rates impact this analysis? In addition to reviewing the current literature and case law on voting machine standardization, I also present an unrecognized and undocumented connection between the “all deliberate speed” order in Brown and the Court’s discussion of voting technology in Bush v. Gore

Affirming Michigan\u27s Action: The Michigan Journal of Race & Law\u27s Response to Dr. Carcieri\u27s Grutter v. Bollinger and Civil Disobedience

One of two articles in this issue on Grutter v. Bollinger; this is a response to Martin D. Carcieri\u27s article Grutter v. Bollinger and Civil Disobedience

Extracellular Calcium Modulates Actions of Orthosteric and Allosteric Ligands on Metabotropic Glutamate Receptor 1alpha

SUMMARY: Metabotropic glutamate receptor 1α (mGluR1α), a member of the family C G protein-coupled receptors (GPCRs), is emerging as a potential drug target for various disorders including chronic neuronal degenerative diseases. In addition to being activated by glutamate, mGluR1α is also modulated by extracellular Ca2+. However, the underlying mechanism is unknown. Moreover, it has long been challenging to develop receptor-specific agonists due to homologies within the mGluR family, and the Ca2+-binding site(s) on mGluR1α may provide an opportunity for receptor-selective targeting by therapeutics. In the present study, we show that our previously predicted Ca2+-binding site in the hinge region of mGluR1α is adjacent to the site where orthosteric agonists and antagonists bind on the extracellular domain of the receptor. Moreover, we have found that extracellular Ca2+ enhances mGluR1α-mediated intracellular Ca2+ responses evoked by the orthosteric agonist, L-quisqualate. Conversely, extracellular Ca2+ diminishes the inhibitory effect of the mGluR1α orthosteric antagonist, (s)-MCPG. In addition, selective positive (Ro 67-4853) and negative (CPCCOEt) allosteric modulators of mGluR1α potentiate and inhibit responses to extracellular Ca2+, respectively, in a manner similar to their effects on the response of mGluR1α to glutamate. Mutations at residues predicted to be involved in Ca2+-binding, including E325I, have significant effects on the modulation of responses to the orthosteric agonist, L-quisqualate, and the allosteric modulator Ro 67-4853 by extracellular Ca2+. These studies reveal that binding of extracellular Ca2+ to the predicted Ca2+-binding site in the ECD of mGluR1α modulates not only glutamate-evoked signaling but also the actions of both orthosteric ligands and allosteric modulators on mGluR1α

Effect of Novel Dietary Supplement on Metabolism in \u3cem\u3evitro\u3c/em\u3e and \u3cem\u3ein vivo\u3c/em\u3e

Obesity is an increasingly prevalent and preventable morbidity with multiple behavioral, surgical and pharmacological interventions currently available. Commercial dietary supplements are often advertised to stimulate metabolism and cause rapid weight and/or fat loss, although few well-controlled studies have demonstrated such effects. We describe a commercially available dietary supplement (purportedly containing caffeine, catechins, and other metabolic stimulators) on resting metabolic rate in humans, and on metabolism, mitochondrial content, and related gene expression in vitro. Human males ingested either a placebo or commercially available supplement (RF) in a randomized double-blind placebo-controlled cross-over fashion. Metabolic rate, respiratory exchange ratio, and blood pressure were measured hourly for 3 h post-ingestion. To investigate molecular effects, human rhabdomyosarcoma cells (RD) and mouse myocytes (C2C12) were treated with various doses of RF for various durations. RF enhanced energy expenditure and systolic blood pressure in human males without altering substrate utilization. In myocytes, RF enhanced metabolism, metabolic gene expression, and mitochondrial content suggesting RF may target common energetic pathways which control mitochondrial biogenesis. RF appears to increase metabolism immediately following ingestion, although it is unclear if RF provides benefits beyond those provided by caffeine alone. Additional research is needed to examine safety and efficacy for human weight loss