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 temporal characteristics of inflammatory cell infiltration and cytokineon OVA-induced mouse lung.

<p>The samples were collected 0, 1 h, 8 h, 1 d, 2 d and 4 d after OVA challenge. (A) The inflammatory infiltrates (arrows) in the peribronchial (HE-Br) and perivessel (HE-Ve) tissues gradually increased in a time-dependent manner. The airway inflammation scores were based on HE staining of the peribronchial (HE-Br) and perivessel (HE-Ve) tissues (B). The IL-4, IL-5, and IL-13 levels were detected in the BALF (C) and OVA-specific IgE (D) was detected in the serum. The original magnification was × 200. Mean ± SEM. *, P < .05; **, P < .01; ***, P < .001. N = 6 in each group. Results are representative of two independent experiments.</p

Airway hyper-reactivity determination and airway inflammation in the lung of asthma mice.

<p>The animals were sacrificed on day 25 to determine tissue inflammation and on day 26 for airway hyper-reactivity (AHR). (A) The OVA/OVA mice presented a remarkably high airway responsiveness to increasing metacholine (Mch) doses (6.25, 12.5, 25, 50 and 100 mg/ml). *, P < .05; ***, P < .001 compared with the control group at the same Mch concentration. (B) PC100 and PC200 were obtained by linear interpolation of the concentration response curve between the final two doses of the respective provocative agent. (C) Representative H&E, PAS and Masson’s stained lung section photomicrographs are shown for each group. The OVA/OVA mice showed apparent inflammatory infiltrates (yellow arrows), including peribronchial (HE-Br) and perivessel (HE-Ve) inflammation, swollen bronchial epithelial cells with increased mucus (green arrows), numerous mucus-containing cells (PAS, black arrows) and collagen deposition (white arrows, blue staining for Masson’s) compared with the PBS/PBS mice. The original magnification was ×200. (D) The airway inflammation scores were based on the HE and PAS staining. The HE total represented the scores from HE stains from both peribronchial and perivessel cells. (E) Cell counts were obtained from the total inflammatory cells, eosinophils, macrophages, lymphocytes and neutrophils in the BALF. Mean ± SEM. *, P < .05; **, P < .01; ***, P < .001 compared with the PBS/PBS group. AHR, airway hyper-reactivity. BALF, bronchoalveolar lavage fluid; H&E, hematoxylin and eosin; HE(Br), HE stain peribronchial; HE(Ve), HE stain perivessel; OVA, ovalbumin; PAS, periodic acid—Schiff; PBS, phosphate-buffered saline; Pech%, the percent changes of Pech from corresponding baseline values; PC100, increased Penh to 100% of baseline; PC200, increased Penh to 200% of baseline. N = 6 mice for each group. Results are representative of three independent experiments.</p

A mouse model of OVA-induced asthma.

<p>For sensitization, BALB/c mice received an i.p injection of OVA or PBS with aluminum hydroxide on days 1, 7 and 14. From days 21 to 25, the mice were challenged with aerosolized 5% OVA or PBS in a plexiglass chamber for 30 minutes per day. Samples were collected on day 25. PBS, phosphate-buffered saline; i.p, intraperitoneal; OVA, ovalbumin.</p

OVA induced increased BALF Th2 cytokine levels and serum Ig protein levels.

<p>(A) BALF IL-4, IL-5 and IL-13 levels. (B) Serum IgE, IgG1 and IgG2a levels. Mean ± SEM. *, P < .05; **, P < .01; ***, P < .001. N = 6 in each group. Results are representative of three independent experiments.</p

The correlation between the Cx43 levels and lung inflammation, interleukin and IgE levels.

<p>(A) The correlation between Cx43 protein levels and the inflammatory HE-Br and HE-Ve scores. The correlation between Cx43 protein levels and the IL-4, IL-5, and IL-13 levels in the BALF (B), and OVA-specific IgE levels in the serum (C). The dots represent the average HE scores or cytokine and IgE levels (Y axis), and Cx43 protein levels detected by western blot (X axis). Cx43 protein levels were analyzed at each time point after the first challenge relative to the 0 h time point in the control group (n = 6 in each group). Results are representative of two independent experiments.</p