1,294 research outputs found
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An Adaptive Load Balance and Handoff Management Strategy for Hierarchical Infrastructure Networks
Hierarchical cellular networks that employ microcells with overlaying macrocells have been proposed to increase the traffic-carrying capacity and circuit quality. Variations in the traffic loads among cells will lessen the traffic-carrying capacity. Moreover, the handoff procedure usually takes place when the call crosses the cell boundary. An ineffective management will increase the system overheads, such as channel switch, data switch, and even network switch. The invetigation proposes an effective load balance and handoff management strategy. This strategy are implemented to solve traffic-adaption problem that can enhance the traffic-carrying capacity for variations in traffic. For the management of handoff procedure, our strategy considers the mobility of mobile hosts and the bandwidth utilization in macrocells. It can descrease the number of handoffs and, accordingly, lessen the system overhead. Furthermore, the simulation results are presented to confirm the efficiency of the proposed strategy
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Performance of Energy Efficient Relaying for Cluster-Based Wireless Sensor Networks
This paper proposes a novel energy efficient data relaying scheme to improve energy efficiency for cluster-based wireless sensor networks (WSNs). In order to reduce the energy dissipation of transmitting sensing data at each sensor, the fixed clustering algorithm uniformly divides the sensing area into clusters where the cluster head is deployed to the centered of the cluster area. Moreover, to perform energy efficient data relaying fixed clustering (EERFC), the cluster head is deployed as close to the sink as possible. Simulation results show that proposed EERFC definitely reduces the energy consumption of the sensors and it can further efficiently relay the cluster data
Ractopamine at the Center of Decades-Long Scientific and Legal Disputes: A Lesson on Benefits, Safety Issues, and Conflicts
Ractopamine (RAC) is a synthetic phenethanolamine, β–adrenergic agonist used as a feed additive to develop leanness and increase feed conversion efficiency in different farm animals. While RAC has been authorized as a feed additive for pigs and cattle in a limited number of countries, a great majority of jurisdictions, including the European Union (EU), China, Russia, and Taiwan, have banned its use on safety grounds. RAC has been under long scientific and political discussion as a controversial antibiotic as a feed additive. Here, we will present significant information on RAC regarding its application, detection methods, conflicts, and legal divisions that play a major role in controversial deadlock and why this issue warrants the attention of scientists, agriculturists, environmentalists, and health advocates. In this review, we highlight the potential toxicities of RAC on aquatic animals to emphasize scientific evidence and reports on the potentially harmful effects of RAC on the aquatic environment and human health
Infrared Studies of Molecular Shocks in the Supernova Remnant HB 21: II. Thermal Admixture of Shocked H Gas in the South
We present near- and mid-infrared observations on the shock-cloud interaction
region in the southern part of the supernova remnant HB 21, performed with the
InfraRed Camera (IRC) aboard AKARI satellite and the Wide InfraRed Camera
(WIRC) at the Palomar 5 m telescope. The IRC 4 um (N4), 7 um (S7), and 11 um
(S11) band images and the WIRC H2 v=1->0 S(1) 2.12 um image show similar
diffuse features, around a shocked CO cloud. We analyzed the emission through
comparison with the H2 line emission of several shock models. The IRC colors
are well explained by the thermal admixture model of H2 gas--whose
infinitesimal H2 column density has a power-law relation with the temperature
, --with n(H2) cm^{-2}, , and
N(H2;T>100K) cm^{-2}. We interpreted these parameters
with several different pictures of the shock-cloud interactions--multiple
planar C-shocks, bow shocks, and shocked clumps--and discuss their weaknesses
and strengths. The observed H2 v=1->0 S(1) intensity is four times greater than
the prediction from the power-law admixture model, the same tendency as found
in the northern part of HB 21 (Paper I). We also explored the limitation of the
thermal admixture model with respect to the derived model parameters.Comment: 35 pages, 10 figures, Accepted in "Advances in Space Research",
higher resolution @
http://astro.snu.ac.kr/~jhshinn/asr-20090921-submitted_arxiv.pdf ; rev.2 -
deletion of section 6.4 and the related content
Common Variants in the Glycerol Kinase Gene Reduce Tuberculosis Drug Efficacy
Despite the administration of multiple drugs that are highly effective in vitro, tuberculosis (TB) treatment requires prolonged drug administration and is confounded by the emergence of drug-resistant strains. To understand the mechanisms that limit antibiotic efficacy, we performed a comprehensive genetic study to identify Mycobacterium tuberculosis genes that alter the rate of bacterial clearance in drug-treated mice. Several functionally distinct bacterial genes were found to alter bacterial clearance, and prominent among these was the glpK gene that encodes the glycerol-3-kinase enzyme that is necessary for glycerol catabolism. Growth on glycerol generally increased the sensitivity of M. tuberculosis to antibiotics in vitro, and glpK-deficient bacteria persisted during antibiotic treatment in vivo, particularly during exposure to pyrazinamide-containing regimens. Frameshift mutations in a hypervariable homopolymeric region of the glpK gene were found to be a specific marker of multidrug resistance in clinical M. tuberculosis isolates, and these loss-of-function alleles were also enriched in extensively drug-resistant clones. These data indicate that frequently observed variation in the glpK coding sequence produces a drug-tolerant phenotype that can reduce antibiotic efficacy and may contribute to the evolution of resistance.
IMPORTANCE: TB control is limited in part by the length of antibiotic treatment needed to prevent recurrent disease. To probe mechanisms underlying survival under antibiotic pressure, we performed a genetic screen for M. tuberculosis mutants with altered susceptibility to treatment using the mouse model of TB. We identified multiple genes involved in a range of functions which alter sensitivity to antibiotics. In particular, we found glycerol catabolism mutants were less susceptible to treatment and that common variation in a homopolymeric region in the glpK gene was associated with drug resistance in clinical isolates. These studies indicate that reversible high-frequency variation in carbon metabolic pathways can produce phenotypically drug-tolerant clones and have a role in the development of resistance
Second-Hand Smoke–Induced Cardiac Fibrosis Is Related to the Fas Death Receptor Apoptotic Pathway without Mitochondria-Dependent Pathway Involvement in Rats
Exposure to environmental tobacco smoke has been epidemiologically linked to heart disease among nonsmokers. However, the molecular mechanism behind the pathogenesis of cardiac disease is unknown. In this study, we found that Wistar rats, exposed to tobacco cigarette smoke at doses of 5, 10, or 15 cigarettes for 30 min twice a day for 1 month, had a dose-dependently reduced heart weight to body weight ratio and enhanced interstitial fibrosis as identified by histopathologic analysis. The mRNA and activity of matrix metalloprotease-2 (MMP-2), representing the progress of cardiac remodeling, were also elevated in the heart. In addition, we used reverse-transcriptase polymerase chain reaction and Western blotting to demonstrate significantly increased levels of the apoptotic effecter caspase-3 in treated animal hearts. Dose-dependently elevated mRNA and protein levels of Fas, and promoted apoptotic initiator caspase-8 (active form), a molecule of a death-receptor–dependent pathway, coupled with unaltered or decreased levels of cytosolic cytochrome c and the apoptotic initiator caspase-9 (active form), molecules of mitochondria-dependent pathways, may be indicative of cardiac apoptosis, which is Fas death-receptor apoptotic-signaling dependent, but not mitochondria pathway dependent in rats exposed to second-hand smoke (SHS). With regard to the regulation of survival pathway, using dot blotting, we found cardiac insulin-like growth factor-1 (IGF-1) and IGF-1 receptor mRNA levels to be significantly increased, indicating that compensative effects of IGF-1 survival signaling could occur. In conclusion, we found that the effects of SHS on cardiomyocyte are mediated by the Fas death-receptor–dependent apoptotic pathway and might be related to the epidemiologic incidence of cardiac disease of SHS-exposed non-smokers
Pulmonary Toxicity after a Quick Course of Combinatorial Vincristine, Bleomycin, and Cisplatin Neoadjuvant Chemotherapy in Cervical Cancer
Pulmonary toxicity is one of the most serious adverse effects associated with a quick course of vincristine, bleomycin, and cisplatin neoadjuvant chemotherapy (NAC-VBP). The aim of this study was to evaluate pulmonary toxicity related to a quick course NAC-VBP. A total of consecutive 61 patients, who underwent at most 3 cycles of NAC-VBP every 10 days in the International Federation of Gynecology and Obstetrics (FIGO) stage IB-IIB cervical cancer from 1995 to 2007, were retrospectively analyzed. Of the 61 study subjects, 7 (11.5%) were identified to have pulmonary toxicity and 2 (3.3%) died of pulmonary fibrosis progression despite aggressive treatment and the use of a multidisciplinary approach. No factor predisposing pulmonary toxicity was identified. Initial symptoms were non-specific, but bronchiolitis obliterans organizing pneumonia and interstitial pneumonitis were characteristic findings by high-resolution computed tomography of the chest. The benefit of steroid therapy was uncertain and was associated with steroid-induced diabetes mellitus requiring insulin therapy in two patients. Fatal pulmonary toxicity is a major concern of a quick course NAC-VBP. In conclusion, these patients require special monitoring for bleomycin-induced pulmonary toxicity
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