3,655 research outputs found

    NQAR: Network Quality Aware Routing in Error-Prone Wireless Sensor Networks

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    We propose a network quality aware routing (NQAR) mechanism to provide an enabling method of the delay-sensitive data delivery over error-prone wireless sensor networks. Unlike the existing routing methods that select routes with the shortest arrival latency or the minimum hop count, the proposed scheme adaptively selects the route based on the network qualities including link errors and collisions with minimum additional complexity. It is designed to avoid the paths with potential noise and collision that may cause many non-deterministic backoffs and retransmissions. We propose a generic framework to select a minimum cost route that takes the packet loss rate and collision history into account. NQAR uses a data centric approach to estimate a single-hop delay based on processing time, propagation delay, packet loss rate, number of backoffs, and the retransmission timeout between two neighboring nodes. This enables a source node to choose the shortest expected end-to-end delay path to send a delay-sensitive data. The experiment results show that NQAR reduces the end-to-end transfer delay up to approximately 50% in comparison with the latency-based directed diffusion and the hop count-based directed diffusion under the error-prone network environments. Moreover, NQAR shows better performance than those routing methods in terms of jitter, reachability, and network lifetime

    Inhibition of c-Jun NH(2)-terminal kinase or extracellular signal-regulated kinase improves lung injury

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    BACKGROUND: Although in vitro studies have determined that the activation of mitogen-activated protein (MAP) kinases is crucial to the activation of transcription factors and regulation of the production of proinflammatory mediators, the roles of c-Jun NH(2)-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) in acute lung injury have not been elucidated. METHODS: Saline or lipopolysaccharide (LPS, 6 mg/kg of body weight) was administered intratracheally with a 1-hour pretreatment with SP600125 (a JNK inhibitor; 30 mg/kg, IO), or PD98059 (an MEK/ERK inhibitor; 30 mg/kg, IO). Rats were sacrificed 4 hours after LPS treatment. RESULTS: SP600125 or PD98059 inhibited LPS-induced phosphorylation of JNK and ERK, total protein and LDH activity in BAL fluid, and neutrophil influx into the lungs. In addition, these MAP kinase inhibitors substantially reduced LPS-induced production of inflammatory mediators, such as CINC, MMP-9, and nitric oxide. Inhibition of JNK correlated with suppression of NF-κB activation through downregulation of phosphorylation and degradation of IκB-α, while ERK inhibition only slightly influenced the NF-κB pathway. CONCLUSION: JNK and ERK play pivotal roles in LPS-induced acute lung injury. Therefore, inhibition of JNK or ERK activity has potential as an effective therapeutic strategy in interventions of inflammatory cascade-associated lung injury

    Target-controlled infusion of remimazolam effect-site concentration for total intravenous anesthesia in patients undergoing minimal invasive surgeries

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    BackgroundAlthough pharmacokinetic and pharmacodynamic models of remimazolam have been developed, their clinical application remains limited. This study aimed to administer a target-controlled infusion (TCI) of remimazolam at the effect-site concentration (Ce) in patients undergoing general anesthesia and to investigate the relationship of the remimazolam Ce with sedative effects and with recovery from general anesthesia.MethodsFifty patients aged 20–75 years, scheduled for minimally invasive surgery under general anesthesia for less than 2 h, were enrolled. Anesthesia was induced and maintained using Schüttler’s model for effect-site TCI of remimazolam. During induction, the remimazolam Ce was increased stepwise, and sedation levels were assessed using the Modified Observer’s Assessment of Alertness/Sedation (MOAA/S) scale and bispectral index (BIS). Following attainment of MOAA/S scale 1, continuous infusion of remifentanil was commenced, and rocuronium (0.6 mg/kg) was administered for endotracheal intubation. The target Ce of remimazolam and the remifentanil infusion rate were adjusted to maintain a BIS between 40 and 70 and a heart rate within 20% of the baseline value. Approximately 5 min before surgery completion, the target Ce of remimazolam was reduced by 20–30%, and anesthetic infusion ceased at the end of surgery. Nonlinear mixed-effects modeling was employed to develop pharmacodynamic models for each sedation level as well as emergence from anesthesia.ResultsThe remimazolam Ces associated with 50% probability (Ce50) of reaching MOAA/S scale ≤4, 3, 2, and 1 were 0.302, 0.397, 0.483, and 0.654 μg/mL, respectively. The Ce50 values for recovery of responsiveness (ROR) and endotracheal extubation were 0.368 and 0.345 μg/mL, respectively. The prediction probabilities of Ce and BIS for detecting changes in sedation level were 0.797 and 0.756, respectively. The sedation scale significantly correlated with remimazolam Ce (r = −0.793, P < 0.0001) and BIS (r = 0.914, P < 0.0001). Age significantly correlated with Ce at MOAA/S1 and ROR.ConclusionEffect-site TCI of remimazolam was successfully performed in patients undergoing general anesthesia. The remimazolam Ce significantly correlated with sedation depth. The Ce50 for MOAA/S scale ≤1 and ROR were determined to be 0.654 and 0.368 μg/mL, respectively

    Identification of H3K4me1-associated proteins at mammalian enhancers.

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    Enhancers act to regulate cell-type-specific gene expression by facilitating the transcription of target genes. In mammalian cells, active or primed enhancers are commonly marked by monomethylation of histone H3 at lysine 4 (H3K4me1) in a cell-type-specific manner. Whether and how this histone modification regulates enhancer-dependent transcription programs in mammals is unclear. In this study, we conducted SILAC mass spectrometry experiments with mononucleosomes and identified multiple H3K4me1-associated proteins, including many involved in chromatin remodeling. We demonstrate that H3K4me1 augments association of the chromatin-remodeling complex BAF to enhancers in vivo and that, in vitro, H3K4me1-marked nucleosomes are more efficiently remodeled by the BAF complex. Crystal structures of the BAF component BAF45C indicate that monomethylation, but not trimethylation, is accommodated by BAF45C's H3K4-binding site. Our results suggest that H3K4me1 has an active role at enhancers by facilitating binding of the BAF complex and possibly other chromatin regulators

    A standardized formula for aesthetic mandibular reconstruction using an osteocutaneous fibular free flap

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    Ameloblastoma is the most common benign odontogenic tumor of the jaw, and expansional growth of a huge untreated ameloblastoma can result in disturbances in facial aesthetics and function, such as difficulty with mouth opening, swallowing, chewing, breathing, neurologic deficits, and pathologic fractures. Radical wide resection with safety margins and subsequent reconstruction is generally recommended. A fibular free flap (FFF) is commonlyused to reconstruct the mandible in order to adequately restore both aesthetic appearance and function. The aim of this brief clinical report is to present a case of huge ameloblastoma after wide resection with free safety margins, and describe the immediate one-step mandibular reconstruction using a vascularized composite FFF. The sterolithographic(rapid prototype, RP) model, a wax pattern of the resected mandible, and a surgical fibular stent made from the wax pattern were constructed preoperatively. We suggest a standardized surgical protocol for mandibular reconstruction with FFF.Funding: Supported by the International Research & Development Program of the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT & Future Planning (NRF-2015K1A3A9A01028230)Keywords: Mandibular reconstruction, fibular osteocutaneous free flap, huge ameloblastoma, stereolithographicmodel, standardized formul

    HRT, Herbal Formula, Induces G 2

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    We have demonstrated the anticancer effect of HRT in HCT116, human colon carcinoma cells. HRT inhibited cancer cell growth by causing cell cycle arrest at G2/M and inducing apoptosis as evidenced by DNA fragmentation assay. We found that HRT induces the activation of caspase-3, -8, and -9, whereas it reduces the level of Bcl-2 protein and results in the cleavage of PARP. Further, HRT decreased the level of phosphorylation of Akt and its downstream signals such as mTOR and GSK-3β. These results indicate that HRT stimulates the apoptotic signaling pathway and represses the survival and proliferation of colon cancer cells via inhibiting Akt activity. Hence, our results suggest that HRT has a potential to be developed as a therapeutic agent against colon cancer cells
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