Abstract-This paper proposes S-MAC, a medium access control (MAC) protocol designed for wireless sensor networks. Wireless sensor networks use battery-operated computing and sensing devices. A network of these devices will collaborate for a common application such as environmental monitoring. We expect sensor networks to be deployed in an ad hoc fashion, with nodes remaining largely inactive for long time, but becoming suddenly active when something is detected. These characteristics of sensor networks and applications motivate a MAC that is different from traditional wireless MACs such as IEEE 802.11 in several ways: energy conservation and self-configuration are primary goals, while per-node fairness and latency are less important. S-MAC uses a few novel techniques to reduce energy consumption and support self-configuration. It enables low-duty-cycle operation in a multihop network. Nodes form virtual clusters based on common sleep schedules to reduce control overhead and enable traffic-adaptive wake-up. S-MAC uses in-channel signaling to avoid overhearing unnecessary traffic. Finally, S-MAC applies message passing to reduce contention latency for applications that require in-network data processing. The paper presents measurement results of S-MAC performance on a sample sensor node, the UC Berkeley Mote, and reveals fundamental tradeoffs on energy, latency and throughput. Results show that S-MAC obtains significant energy savings compared with an 802.11-like MAC without sleeping.Index Terms-Energy efficiency, medium access control (MAC), sensor network, wireless network.

Modern development of chemical manufacturing requires a substantial reduction in energy consumption and catalyst cost. Sunlight-driven chemical transformation by metal oxides holds great promise for this goal; however, it remains a grand challenge to efficiently couple solar energy into many catalytic reactions. Here we report that defect engineering on oxide catalyst can serve as a versatile approach to bridge light harvesting with surface reactions by ensuring species chemisorption. The chemisorption not only spatially enables the transfer of photoexcited electrons to reaction species, but also alters the form of active species to lower the photon energy requirement for reactions. In a proof of concept, oxygen molecules are activated into superoxide radicals on defect-rich tungsten oxide through visible-near-infrared illumination to trigger organic aerobic couplings of amines to corresponding imines. The excellent efficiency and durability for such a highly important process in chemical transformation can otherwise be virtually impossible to attain by counterpart materials.

Photocatalysis may provide an intriguing approach to nitrogen fixation, which relies on the transfer of photoexcited electrons to the ultrastable N≡N bond. Upon N chemisorption at active sites (e.g., surface defects), the N molecules have yet to receive energetic electrons toward efficient activation and dissociation, often forming a bottleneck. Herein, we report that the bottleneck can be well tackled by refining the defect states in photocatalysts via doping. As a proof of concept, WO ultrathin nanowires are employed as a model material for subtle Mo doping, in which the coordinatively unsaturated (CUS) metal atoms with oxygen defects serve as the sites for N chemisorption and electron transfer. The doped low-valence Mo species play multiple roles in facilitating N activation and dissociation by refining the defect states of WO: (1) polarizing the chemisorbed N molecules and facilitating the electron transfer from CUS sites to N adsorbates, which enables the N≡N bond to be more feasible for dissociation through proton coupling; (2) elevating defect-band center toward the Fermi level, which preserves the energy of photoexcited electrons for N reduction. As a result, the 1 mol % Mo-doped WO sample achieves an ammonia production rate of 195.5 μmol g h, 7-fold higher than that of pristine WO. In pure water, the catalyst demonstrates an apparent quantum efficiency of 0.33% at 400 nm and a solar-to-ammonia efficiency of 0.028% under simulated AM 1.5 G light irradiation. This work provides fresh insights into the design of photocatalyst lattice for N fixation and reaffirms the versatility of subtle electronic structure modulation in tuning catalytic activity.

Zebularine is a stable DNA demethylating agent and the first drug in its class able to reactivate an epigenetically silenced gene by oral administration.

No abstract

Energy is a critical resource in sensor networks. MAC protocols such as S-MAC and T-MAC coordinate sleep schedules to reduce energy consumption. Recently, lowpower listening (LPL) approaches such as WiseMAC and B-MAC exploit very brief polling of channel activity combined with long preambles before each transmission, saving energy particularly during low network utilization. Synchronization cost, either explicitly in scheduling, or implicitly in long preambles, limits all these protocols to duty cycles of 1-2%. We demonstrate that ultra-low duty cycles of 0.1% and below are possible with a new MAC protocol called scheduled channel polling (SCP). This work prompts three new contributions: First, we establish optimal configurations for both LPL and SCP under fixed conditions, developing a lower bound of energy consumption. Under these conditions, SCP can extend lifetime of a network by a factor of 3-6 times over LPL. Second, SCP is designed to adapt well to variable traffic. LPL is optimized for known, periodic traffic, and long preambles become very costly when traffic varies. In one experiment, SCP reduces energy consumption by a factor of 10 under bursty traffic. We also show how SCP adapts to heavy traffic and streams data in multi-hop networks, reducing latency by 85% and energy by 95% at 9 hops. Finally, we show that SCP can operate effectively on recent hardware such as 802.15.4 radios. In fact, power consumption of SCP decreases with faster radios, but that of LPL increases.

The unfolded protein response (UPR) is an evolutionarily conserved mechanism that activates both proapoptotic and survival pathways to allow eukaryotic cells to adapt to endoplasmic reticulum (ER) stress. Although the UPR has been implicated in tumorigenesis, its precise role in endogenous cancer remains unclear. A major UPR protective response is the induction of the ER chaperone GRP78/BiP, which is expressed at high levels in a variety of tumors and confers drug resistance in both proliferating and dormant cancer cells. To determine the physiologic role of GRP78 in in situ-generated tumor and the consequence of its suppression on normal organs, we used a genetic model of breast cancer in the Grp78 heterozygous mice where GRP78 expression level was reduced by about half, mimicking anti-GRP78 agents that achieve partial suppression of GRP78 expression. Here, we report that Grp78 heterozygosity has no effect on organ development or antibody production but prolongs the latency period and significantly impedes tumor growth. Our results reveal three major mechanisms mediated by GRP78 for cancer progression: enhancement of tumor cell proliferation, protection against apoptosis, and promotion of tumor angiogenesis. Importantly, although partial reduction of GRP78 in the Grp78 heterozygous mice substantially reduces the tumor microvessel density, it has no effect on vasculature of normal organs. Our findings establish that a key UPR target GRP78 is preferably required for pathophysiologic conditions, such as tumor proliferation, survival, and angiogenesis, underscoring its potential value as a novel therapeutic target for dual antitumor and antiangiogenesis activity. [Cancer Res 2008; 68(2):498-505]

Cancer stem cells (CSCs) play critical roles in cancer initiation, progression, and therapeutic refractoriness. Although many studies have focused on the genes and pathways involved in stemness, characterization of the factors in the tumor microenvironment that regulate CSCs is lacking. In this study, we investigated the effects of stromal fibroblasts on breast cancer (BC) stem cells. We found that compared to normal fibroblasts, primary cancer-associated fibroblasts (CAFs) and fibroblasts activated by co-cultured BC cells produce higher levels of chemokine (C-C motif) ligand 2 (CCL2), which stimulates the stem cell-specific, sphere-forming phenotype in BC cells and CSC self-renewal. Increased CCL2 expression in activated fibroblasts required STAT3 activation by diverse BC-secreted cytokines, and in turn, induced NOTCH1 expression and the CSC features in BC cells, constituting a “cancer-stroma-cancer” signaling circuit. In a xenograft model of paired fibroblasts and BC tumor cells, loss of CCL2 significantly inhibited tumorigenesis and NOTCH1 expression. In addition, upregulation of both NOTCH1 and CCL2 was associated with poor differentiation in primary BCs, further supporting the observation that NOTCH1 is regulated by CCL2. Our findings therefore suggest that CCL2 represents a potential therapeutic target that can block the cancer-host communication that prompts CSC-mediated disease progression.