Power consumption variability of both on-chip SRAMs and off-chip DRAMs is expected to continue to increase over the next decades. We opportunistically exploit this variability through a novel Variabilityaware Memory Virtualization (VaMV) layer that allows programmers to partition their application's address space (through annotations) into virtual address regions and create mapping policies for each region. Each policy has different requirements (e.g., power, fault-tolerance) and is exploited by our dynamic memory management module (VaMVisor), which adapts to the underlying hardware, prioritizes the memory resources according to their characteristics (e.g., power consumption), and selectively maps data to the best-fitting memory resource (e.g., high-utilization data to low-power memory space). Our experimental results on embedded benchmarks show that VaMV is capable of reducing dynamic power consumption by 63% on average while reducing total execution time by an average of 34% by exploiting: 1) SRAM voltage scaling, 2) DRAM power variability, and 3) Efficient dynamic policydriven variability-aware memory allocation.

Jervell and Lange-Nielsen syndrome (MIM 220400; JLNS), is a rare form of profound congenital deafness combined with syncopal attacks and sudden death due to prolonged QTc; it is an autosomal recessive trait. After its first description in Norway in 1957, later reports from many other countries have confirmed its occurrence. Nowhere is the prevalence so high as in Norway, where we estimate a prevalence of at least 1:200,000. The KCNQ1 and KCNE1 proteins coassemble in a potassium channel, and mutations in either the KCNQ1 gene or the KCNE1 gene disrupt endolymph production in the stria vascularis in the cochlea, causing deafness. KCNQ1 seems to be the major gene in JLNS. Long QT syndrome (LQTS) is a separate disorder of either autosomal dominant or recessive inheritance caused by mutations in four different ion channel genes; KCNQ1 is the one most frequently involved. Some heterozygous carriers of JLNS mutations in either gene may suffer from prolonged QTc and be symptomatic LQTS patients with a need for appropriate medical treatment to prevent life-threatening cardiac arrhythmia. In general, frameshift/stop mutations cause JLNS, and missense/splice site mutations cause LQTS, but a precise genotype-phenotype correlation in LQTS and JLNS is not established, which complicates both genetic counseling and clinical risk evaluation in carriers. We review JLNS from a Norwegian perspective because of the unusually high prevalence, the genetic homogeneity associated with considerable mutational heterogeneity, and some evidence for recurrent mutational events as well as one founder mutation. We outline the clinical implications for investigation of deaf children and cases of sudden infant death syndrome as well as careful electrocardiographic monitoring of identified mutation carriers to prevent sudden death. Am. J. Med. Genet. (Semin. Med. Genet.) 89:137-146, 1999.

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