An Analog Baseband Approach for Designing Full-Duplex Radios

Recent wireless testbed implementations have proven that full-duplex communication is in fact possible and can outperform half-duplex systems. Many of these implementations modify existing half-duplex systems to operate in full-duplex. To realize the full potential of full-duplex, radios need to be designed with self-interference in mind. In our work, we use an experimental setup with a patch antenna prototype to characterize the self-interference channel between two radios. In doing so, we form an analytical model to design analog baseband cancellation techniques. We show that our cancellation scheme can provide up to 10 dB improved signal strength, 2.5 bps/Hz increase in rate, and a 10,000 improvement in BER as compared to the RF only cancellation provided by the patch antenna.Comment: 5 pages, 8 figures, to appear in 2013 Asilomar Conference proceeding

Seas of Sorrow, Lakes of Heaven: Community and Ishimure Michiko

The goal of this thesis is to examine the theme of community in two translated works, Paradise in the Sea of Sorrow: Our Minamata Disease and Lake of Heaven, by Ishimure Michiko. I analyze how Ishimure defines a community, and I also look at the tension between insiders of the community with outsiders. Next, I look at Ishimure’s use of genre in Paradise in the Sea of Sorrow; she blends autofiction, autobiography, and illness narratives to give different perspectives to reflect on the Minamata disease health crisis. Through this analysis, I also look at the shift in Ishimure’s tone toward outsiders, moving from anger to reconciliation between the texts in question. Lastly, I comment on the change in Ishimure’s public image and discuss a story where she is the outsider experiencing Tokyo

Stallworth Family: Kimberly Hamlett (Youth)

As a child of the ’60s, a person might think Kimberly Hamlett would show signs of her rebellious generation. However, those who know this warm, kindhearted and Christian woman would say differently. Kimberly, born in 1965, was the first child born to her large family. She is the oldest of seven children, four girls and three boys. She was born in Walnut Creek, but grew up in Stockton and continues to live here…https://scholarlycommons.pacific.edu/ss-aa/1005/thumbnail.jp

A function for the mitochondrial chaperonin Hsp60 in the structure and transmission of mitochondrial DNA nucleoids in Saccharomyces cerevisiae

The yeast mitochondrial chaperonin Hsp60 has previously been implicated in mitochondrial DNA (mtDNA) transactions: it is found in mtDNA nucleoids associated with single-stranded DNA; it binds preferentially to the template strand of active mtDNA ori sequences in vitro; and wild-type (ρ+) mtDNA is unstable in hsp60 temperature-sensitive (ts) mutants grown at the permissive temperature. Here we show that the mtDNA instability is caused by a defect in mtDNA transmission to daughter cells. Using high resolution, fluorescence deconvolution microscopy, we observe a striking alteration in the morphology of mtDNA nucleoids in ρ+ cells of an hsp60-ts mutant that suggests a defect in nucleoid division. We show that ρ− petite mtDNA consisting of active ori repeats is uniquely unstable in the hsp60-ts mutant. This instability of ori ρ− mtDNA requires transcription from the canonical promoter within the ori element. Our data suggest that the nucleoid dynamics underlying mtDNA transmission are regulated by the interaction between Hsp60 and mtDNA ori sequences

hnRNPA2 Mediated Acetylation Reduces Telomere Length in Response to Mitochondrial Dysfunction

Telomeres protect against chromosomal damage. Accelerated telomere loss has been associated with premature aging syndromes such as Werner’s syndrome and Dyskeratosis Congenita, while, progressive telomere loss activates a DNA damage response leading to chromosomal instability, typically observed in cancer cells and senescent cells. Therefore, identifying mechanisms of telomere length maintenance is critical for understanding human pathologies. In this paper we demonstrate that mitochondrial dysfunction plays a causal role in telomere shortening. Furthermore, hnRNPA2, a mitochondrial stress responsive lysine acetyltransferase (KAT) acetylates telomere histone H4at lysine 8 of (H4K8) and this acetylation is associated with telomere attrition. Cells containing dysfunctional mitochondria have higher telomere H4K8 acetylation and shorter telomeres independent of cell proliferation rates. Ectopic expression of KAT mutant hnRNPA2 rescued telomere length possibly due to impaired H4K8 acetylation coupled with inability to activate telomerase expression. The phenotypic outcome of telomere shortening in immortalized cells included chromosomal instability (end-fusions) and telomerase activation, typical of an oncogenic transformation; while in non-telomerase expressing fibroblasts, mitochondrial dysfunction induced-telomere attrition resulted in senescence. Our findings provide a mechanistic association between dysfunctional mitochondria and telomere loss and therefore describe a novel epigenetic signal for telomere length maintenance

HnRNPA2 is a Novel Histone Acetyltransferase That Mediates Mitochondrial Stress-Induced Nuclear Gene Expression

Reduced mitochondrial DNA copy number, mitochondrial DNA mutations or disruption of electron transfer chain complexes induce mitochondria-to-nucleus retrograde signaling, which induces global change in nuclear gene expression ultimately contributing to various human pathologies including cancer. Recent studies suggest that these mitochondrial changes cause transcriptional reprogramming of nuclear genes although the mechanism of this cross talk remains unclear. Here, we provide evidence that mitochondria-to-nucleus retrograde signaling regulates chromatin acetylation and alters nuclear gene expression through the heterogeneous ribonucleoprotein A2 (hnRNAP2). These processes are reversed when mitochondrial DNA content is restored to near normal cell levels. We show that the mitochondrial stress-induced transcription coactivator hnRNAP2 acetylates Lys 8 of H4 through an intrinsic histone lysine acetyltransferase (KAT) activity with Arg 48 and Arg 50 of hnRNAP2 being essential for acetyl-CoA binding and acetyltransferase activity. H4K8 acetylation at the mitochondrial stress-responsive promoters by hnRNAP2 is essential for transcriptional activation. We found that the previously described mitochondria-to-nucleus retrograde signaling-mediated transformation of C2C12 cells caused an increased expression of genes involved in various oncogenic processes, which is retarded in hnRNAP2 silenced or hnRNAP2 KAT mutant cells. Taken together, these data show that altered gene expression by mitochondria-to-nucleus retrograde signaling involves a novel hnRNAP2-dependent epigenetic mechanism that may have a role in cancer and other pathologies