Deterministic Relay Networks with State Information

Motivated by fading channels and erasure channels, the problem of reliable communication over deterministic relay networks is studied, in which relay nodes receive a function of the incoming signals and a random network state. An achievable rate is characterized for the case in which destination nodes have full knowledge of the state information. If the relay nodes receive a linear function of the incoming signals and the state in a finite field, then the achievable rate is shown to be optimal, meeting the cut-set upper bound on the capacity. This result generalizes on a unified framework the work of Avestimehr, Diggavi, and Tse on the deterministic networks with state dependency, the work of Dana, Gowaikar, Palanki, Hassibi, and Effros on linear erasure networks with interference, and the work of Smith and Vishwanath on linear erasure networks with broadcast.Comment: 5 pages, to appear in proc. IEEE ISIT, June 200

Endoplasmic Reticulum Stress in the β-Cell Pathogenesis of Type 2 Diabetes

Type 2 diabetes is a complex metabolic disorder characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency by β-cell failure. Even if the mechanisms underlying the pathogenesis of β-cell failure are still under investigation, recent increasing genetic, experimental, and clinical evidence indicate that hyperactivation of the unfolded protein response (UPR) to counteract metabolic stresses is closely related to β-cell dysfunction and apoptosis. Signaling pathways of the UPR are “a double-edged sword” that can promote adaptation or apoptosis depending on the nature of the ER stress condition. In this paper, we summarized our current understanding of the mechanisms and components related to ER stress in the β-cell pathogenesis of type 2 diabetes

Non-monotonic temperature dependent transport in graphene grown by Chemical Vapor Deposition

Temperature-dependent resistivity of graphene grown by chemical vapor deposition (CVD) is investigated. We observe in low mobility CVD graphene device a strong insulating behavior at low temperatures and a metallic behavior at high temperatures manifesting a non-monotonic in the temperature dependent resistivity.This feature is strongly affected by carrier density modulation. To understand this anomalous temperature dependence, we introduce thermal activation of charge carriers in electron-hole puddles induced by randomly distributed charged impurities. Observed temperature evolution of resistivity is then understood from the competition among thermal activation of charge carriers, temperature-dependent screening and phonon scattering effects. Our results imply that the transport property of transferred CVD-grown graphene is strongly influenced by the details of the environmentComment: 7 pages, 3 figure

High-resolution analysis of condition-specific regulatory modules in Saccharomyces cerevisiae

A novel approach for identifying condition-specific regulatory modules in yeast reveals functionally distinct coregulated submodules

CD4+CD25+ regulatory T cells attenuate cisplatin-induced nephrotoxicity in mice

Nephrotoxicity limits the use of cisplatin, a widely used chemotherapeutic agent for treatment of various malignancies. Overall, CD4+ T cells mediate cisplatin-induced renal injury; however, the CD4+CD25+ regulatory T-cell subset (CD4+CD25+ Treg) has broad suppressive effects on many different cell types. In this study, we determined whether CD4+CD25+ Treg cells had protective effects against cisplatin-induced acute renal injury in nu/nu mice that lack mature T cells. In these mice, there was marked attenuation of the decreased survival, renal dysfunction and tubular injury, renal tumor necrosis factor-α, and interleukin-1β cytokine levels. Furthermore, renal macrophage accumulation was reduced in CD4+CD25+ Treg cell-adoptive transferred nu/nu mice compared with control mice. Infusion of CD4+CD25+Treg cells into wild-type Balb/c mice reduced serum blood urea nitrogen and creatinine levels equivalent to those in nu/nu mice and extended their survival time after cisplatin injection. In contrast, depletion of CD4+CD25+ Treg cells in wild-type mice exacerbated kidney injury after cisplatin administration. Transcription factor Foxp3-positive cells (Treg cells) were detected in the kidneys of nu/nu mice after cisplatin injection. Our results suggest that CD4+CD25+ Treg cells directly affect cisplatin nephrotoxicity and their modulation represents an additional treatment strategy