Though the 1960s movement addressed the civil and political rights that were denied to black people—access and use of public accommodations, the right to vote, and ensuring fair employment and housing opportunities—it did not directly confront the racialized degradation black people endured, and many continue to endure, at the hands of the police. What the Black Lives Matter protests have done, however, is not only put police reform on the policy agenda but demanded that American society reconsider how it values black lives.
This past September, during the first week of school, seven-year old Tiana Parker wore dreadlocks tied in a bright pink bow to her school in Tulsa, Oklahoma. The Deborah Brown Community School, a charter school sponsored by the historically black college Langston University, sent Tiana home and told her parents that their child was in violation of a school policy prohibiting students from wearing “unusual hairstyles” that distract from the school’s “respectful” learning environment. Not only were “dreadlocks, Afros, Mohawks” and other so-called faddish styles banned from the school, the school’s handbook also instructed that girls’ “weaved hair should be no longer than shoulder length” and that boys’ hairstyles are “to be short and neatly trimmed.”
Type 2 diabetes mellitus (T2DM) is characterized by defects in haepatic glucose production, insulin action and insulin secretion, which can also lead to a variety of secondary disorders. The disease can lead to death without treatment and it has been predicted that T2DM will affect 215 million people world-wide by 2010. T2DM is a multifactorial condition whose precise genetic causes and biochemical defects have not been fully elucidated but at both levels, calpains appear to play a role. Positional cloning studies mapped T2DM susceptibility to CAPN10, the gene encoding the intracellular cysteine protease, calpain 10. Further studies have shown a number of non-coding polymorphisms in CAPN10 to be functionally associated with T2DM whilst the identification of coding polymorphisms, suggested that mutant calpain 10 proteins may also contribute to the disease. The presence of both calpain 10 and its mRNA have been demonstrated in tissues from several mammalian species whilst calpain 10 appears to be associated with pathways involved in glucose metabolism, insulin secretion and insulin action. It appears that other calpains may also participate in these pathways and here we present an overview of recent studies on calpains and their putative role in T2DM.
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