Modeling Hidden Nodes Collisions in Wireless Sensor Networks: Analysis Approach

This paper studied both types of collisions. In this paper, we show that advocated solutions for coping with hidden node collisions are unsuitable for sensor networks. We model both types of collisions and derive closed-form formula giving the probability of hidden and visible node collisions. To reduce these collisions, we propose two solutions. The first one based on tuning the carrier sense threshold saves a substantial amount of collisions by reducing the number of hidden nodes. The second one based on adjusting the contention window size is complementary to the first one. It reduces the probability of overlapping transmissions, which reduces both collisions due to hidden and visible nodes. We validate and evaluate the performance of these solutions through simulations

The COX-2-Selective Antagonist (NS-398) Inhibits Choroidal Neovascularization and Subretinal Fibrosis

<div><p>Choroidal neovascularization (CNV) is an important pathologic component of neovascular age-related macular degeneration (AMD), and CNV lesions later develop into fibrous scars, which contribute to the loss of central vision. Nowadays, the precise molecular and cellular mechanisms underlying CNV and subretinal fibrosis have yet to be fully elucidated. Cyclooxygenase-2 (COX-2) has previously been implicated in angiogenesis and fibrosis. However, the role of COX-2 in the pathogenesis of CNV and subretinal fibrosis is poorly understood. The present study reveals several important findings concerning the relationship of COX-2 signaling with CNV and subretinal fibrosis. Experimental CNV lesions were attenuated by the administration of NS-398, a COX-2-selective antagonist. NS-398-induced CNV suppression was found to be mediated by the attenuation of macrophage infiltration and down-regulation of VEGF in the retinal pigment epithelium–choroid complex. Additionally, NS-398 attenuated subretinal fibrosis, in an experimental model of subretinal scarring observed in neovascular AMD, by down-regulation of TGF-β₂ in the retinal pigment epithelium–choroid complex. Moreover, we cultured mouse RPE cells and found that NS-398 decreased the secretion of VEGF and TGF-β₂ in mouse RPE cells. The results of the present study provide new findings regarding the molecular basis of CNV and subretinal fibrosis, and provide a proof-of-concept approach for the efficacy of COX-2 inhibition in treating subretinal fibrosis.</p></div

Suppression of CNV with COX-2-selective Antagonist (NS-398).

<p>Representative images of fluorescein dextran perfused RPE–choroidal flat mounts of mice administered PBS vehicle (A), NS-398 intraperitoneally (B), MF1+ DC101 (C) day 10 after photocoagulation. The CNV lesions were assessed quantitatively (D). **<i>P</i><0.001 compared with vehicle-treated mice. Error bars represented ±SD. intraperitoneal vehicle, n = 18 burn spots, intraperitoneal NS-398, n = 20 burn spots, intraperitoneal MF1+ DC101, n = 16 burn spots, Scale bars in A, B,C are 200μm.</p

Suppression of macrophage infiltration with COX-2-selective Antagonist (NS-398).

<p>Green fluorescence from isolectin B4 indicates CNV, red fluorescence indicates F4/80-positive macrophages. Representative macrophage infiltration lesions in the PBS vehicle-treated mice (A) and NS-398-treated mice (B). Areas of F4/80-positive cells were assessed quantitatively (C). **<i>P</i><0.001 compared with vehicle-treated mice. Error bars represented ±SD. intraperitoneal vehicle, n = 15 burn spots, intraperitoneal NS-398, n = 16 burn spots, Scale bars in A, B are 200μm.</p

Suppression of VEGF and TGF-β2 expression with COX-2-selective Antagonist (NS-398) in RPE–choroid complexes and mouse RPE cells.

<p>Light microscope images of confluent RPE cultures on day 10 (A) (magnification = 100×). Immunofluorescence showed Cytokeratin 8-positive cells were the RPE cells (B) (magnification = 400×). In the RPE–choroid complexes, the mRNA and protein levels of VEGF and TGF-β₂ were suppressed significantly in the NS-398-treated mice (4C-4F). *<i>P</i><0.01 compared with vehicle-treated mice for all, after CNV and subretinal fibrosis model formation; vehicle n = 6 eyes for each time point, NS-398 n = 6 eyesfor each time point. In mouse RPE cells, the mRNA and protein levels of VEGF (G, I), TGF-β₂ (H, J) were significantly reduced respectively at 12h, 24h, 36h after added NS-398 (4G-4J). (^#<i>P</i><0.05, *<i>P</i><0.01). Error bars indicate mean ± SD; Experiments were conducted in triplicate with similar results.</p

Three-Dimensional Printing Hollow Polymer Template-Mediated Graphene Lattices with Tailorable Architectures and Multifunctional Properties

It is a significant challenge to concurrently achieve scalable fabrication of graphene aerogels with three-dimensional (3D) tailorable architectures (<i>e.g.,</i> lattice structure) and controllable manipulation of microstructures on the multiscale. Herein, we highlight 3D graphene lattices (GLs) with complex engineering architectures that were delicately designed and manufactured <i><i>via</i></i> 3D stereolithography printed hollow polymer template-mediated hydrothermal process coupled with freeze-drying strategies. The resulting GLs with overhang beams and columns show a 3D geometric configuration with hollow-carved features at the macroscale, while the construction elements of graphene cellular on the microscale exhibit a well-ordered and honeycomb-like microstructure with high porosity. These GLs demonstrate multifunctional properties with robust structure, high electrical conductivity, low thermal conductivity, and superior absorption capacitance of organic solvents. Moreover, the GLs were utilized as a subtle sensor for the fast detection of chemical agents. Aforementioned superior properties of GLs confirm that the combination of 3D tailorable manipulation and self-organization design of structures on the multiscale is an effective strategy for the scalable fabrication of advanced multifunctional graphene monoliths, suggesting their promising applications as chemical detection sensors, environmental remediation absorbers, conductive electrodes, and engineering metamaterials

Suppression of subretinal fibrosis with COX-2-selective Antagonist (NS-398) in a mouse model.

<p>Representative subretinal fibrosis of RPE–choroidal flat mounts of mice administered PBS vehicle (A), NS-398 intraperitoneally (B), on day 7 after PECs-injecting. Subretinal fibrosis lesions were assessed quantitatively(C), **<i>P</i><0.001 compared with vehicle-treated mice. Error bars represented ±SD. intraperitoneal vehicle, n = 16 burn spots, intraperitoneal NS-398, n = 18 burn spots, Scale bars in A, B are 500μm.</p

Data_Sheet_1_Pre-clinical Models for Malignant Mesothelioma Research: From Chemical-Induced to Patient-Derived Cancer Xenografts.XLSX

<p>Malignant mesothelioma (MM) is a rare disease often associated with environmental exposure to asbestos and other erionite fibers. MM has a long latency period prior to manifestation and a poor prognosis. The survival post-diagnosis is often less than a year. Although use of asbestos has been banned in the United States and many European countries, asbestos is still being used and extracted in many developing countries. Occupational exposure to asbestos, mining, and migration are reasons that we expect to continue to see growing incidence of mesothelioma in the coming decades. Despite improvements in survival achieved with multimodal therapies and cytoreductive surgeries, less morbid, more effective interventions are needed. Thus, identifying prognostic and predictive biomarkers for MM, and developing novel agents for targeted therapy, are key unmet needs in mesothelioma research and treatment. In this review, we discuss the evolution of pre-clinical model systems developed to study MM and emphasize the remarkable capability of patient-derived xenograft (PDX) MM models in expediting the pre-clinical development of novel therapeutic approaches. PDX disease model systems retain major characteristics of original malignancies with high fidelity, including molecular, histopathological and functional heterogeneities, and as such play major roles in translational research, drug development, and precision medicine.</p

Assessment rates for EDSS clinical observations (obs) and expected midpoint observations (Exp), by relapsing-onset MS study groups and study periods, Nova Scotia, 1979–2010.

<p>Footnote: obs = an EDSS clinical observation. obs+Exp = obs and expected EDSS measures, assuming midpoint survival time at irreversible disability endpoints.</p

Estimating Typical Multiple Sclerosis Disability Progression Speed from Clinical Observations

<div><p>Introduction</p><p>Multiple sclerosis (MS) is a chronic disease of the central nervous system. Estimates of MS natural history (NH) disability progression speed from clinical observations vary worldwide. This may reflect, in part, variance in censoring-bias) (missing observations) and assumptions about when irreversible disability progression events occurred. We test whether estimates of progression speed which assume midpoint survival time at irreversible disability endpoints are significantly faster than estimates which assume maximum survival time, and are more stable across study groups and time periods.</p><p>Methods</p><p>Our Nova Scotia NH study population includes 2,240 definite relapsing-onset multiple sclerosis (R-MS) natural history patients with 18,078 Expanded Disability Status Scale (EDSS) clinical observations in study period 1979–2010. Progression speed is measured by rate-of-change in range EDSS 0–6 and by survival time at irreversible endpoints EDSS 1–9. Midpoint censoring-bias-reduction methods are applied to clinical observations.</p><p>Findings</p><p>Typical EDSS increase per year in range EDSS 0–6, assuming midpoint survival time, is estimated to be 0.168 for all R-MS, 0.204 for eventually-DMD-treated patients and 0.155 for never-DMD-treated patients. Estimates assuming midpoint rather than maximum survival time are significantly faster: 16% faster for all R-MS natural history patients, 6% faster for eventually-DMD-treated patients, and 21% faster for never-DMD-treated patients. The variability of estimates across study groups and time periods decreased when midpoint survival time was assumed.</p><p>Conclusions</p><p>Estimates of typical disease progression speed from 1979–2010 Nova Scotia clinical observations are sensitive to censoring-bias and to analysts’ survival time assumptions. Censoring-bias-adjusted estimates of typical natural history disability progression speed in relapsing-onset multiple sclerosis patients are significantly faster, and less variable within and across study groups and time periods, than unadjusted estimates, and are, arguably, more relevant for various stakeholders. The application of censoring-bias-reduction methods to other multiple sclerosis clinical databases may reduce variability in estimates of disability progression speed worldwide.</p></div