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The human concentrative nucleoside transporter, CNT3 (SLC28A3), plays an important role in mediating the cellular entry of a broad array of physiological nucleosides and synthetic anticancer nucleoside analog drugs. As a first step toward understanding the genetic basis for interindividual differences in the disposition and response to antileukemic(More)
—This paper presents an ultra-low power batteryless energy harvesting body sensor node (BSN) SoC fabricated in a commercial 130 nm CMOS technology capable of acquiring, processing, and transmitting electrocardiogram (ECG), elec-tromyogram (EMG), and electroencephalogram (EEG) data. This SoC utilizes recent advances in energy harvesting, dynamic power(More)
The AAA-ATPase (ATPase associated with various cellular activities) p97 has been implicated in the degradation of misfolded and unassembled proteins in the endoplasmic reticulum (ERAD). To better understand its role in this process, we used a reconstituted cell-free system to define the precise contribution of p97 in degrading immature forms of the(More)
—This paper presents a low power boost converter for thermoelectric energy harvesting that demonstrates an efficiency that is 15% higher than the state-of-the-art for voltage conversion ratios above 20. This is achieved by utilizing a technique allowing synchronous rectification in the discontinuous conduction mode. A low-power method for input voltage(More)
Fibrillins are large extracellular macromolecules that polymerize to form the backbone structure of connective tissue microfibrils. Mutations in the gene for fibrillin-1 cause the Marfan syndrome, while mutations in the gene for fibrillin-2 cause Congenital Contractural Arachnodactyly. Both are autosomal dominant disorders, and both disorders affect(More)
In humans, mutations in fibrillin-1 result in a variety of genetic disorders with distinct clinical phenotypes. While most of the known mutations in fibrillin-1 cause Marfan syndrome, a number of other mutations lead to clinical features unrelated to Marfan syndrome. Pathogenesis of Marfan syndrome is currently thought to be driven by mechanisms due to(More)
Proteolytic activity of the 20S proteasome is regulated by activators that govern substrate movement into and out of the catalytic chamber. However, the physiological relationship between activators, and hence the relative role of different proteasome species, remains poorly understood. To address this problem, we characterized the total pool of cytosolic(More)
OBJECTIVE To evaluate in a prospective, controlled fashion the prevalence of umbilical artery Doppler waveform notching and its association with cord and placental abnormalities. METHODS During a 6-month period, umbilical artery velocity waveforms were prospectively obtained on 1857 pregnancies at greater than 27 weeks' gestation. All pregnant patients(More)
The 26S proteasome is the primary protease responsible for degrading misfolded membrane proteins in the endoplasmic reticulum. Here we examine the specific role of beta subunit function on polypeptide cleavage and membrane release of CFTR, a prototypical ER-associated degradation substrate with 12 transmembrane segments. In the presence of ATP, cytosol and(More)