ABSTRACT
Delay-tolerant networking (DTN) enables communication in disruptive scenarios where issues such as sparse and intermittent connectivity, long and variable delays, high latency, high error rates, or no end-to-end connectivity exist. Internet of Vehicles (IoV) is a network of the future in which integration between devices, vehicles, and users will be unlimited and universal, overcoming the heterogeneity of systems, services, applications, and devices. Delay-tolerant internet of vehicles (DT-IoV) is emerging and becoming a popular research topic due to the critical applications that can be realized, such as software or map update dissemination. For an IoV to work efficiently, a degree of cooperation between nodes is necessary to deliver messages to their destinations. However, nodes might misbehave and silently drop messages, also known as a black-hole attack, degrading network performance. Various solutions have been proposed to deal with black-hole nodes, but most are centralized or require each node to meet every other node. This paper proposes a decentralized reputation scheme called BiRep that identifies and punishes black-hole nodes in DT-IoV. BiRep is tested on the Prophet routing protocol. Simulation results show excellent performance in all scenarios, comparable or better to other reputation schemes, significantly increasing the delivery ratio of messages.
ABSTRACT
PURPOSE: Idiopathic pulmonary fibrosis (IPF) is a chronic fibrosing interstitial pneumonia, which involves aberrant serotonin (5-hydroxytryptamine [5-HT]) and Akt signaling. As protective effects of chronic aerobic training (AT) have been demonstrated in the context of lung injury, this study investigated whether AT attenuates bleomycin-induced lung fibrosis partly via a reduction of 5-HT and AKT signaling. METHODS: Seventy-two C57BL/6 male mice were distributed in Control (Co), Exercise (Ex), Fibrosis (Fi), and Fibrosis + Exercise (Fi + Ex) groups. Bleomycin (1.5 UI·kg) was administered on day 1 and treadmill AT began on day 15 and continued for 60 min·d, 5 d·wk for 4 wk. We evaluated total and differential cell counts in bronchoalveolar lavage (BAL), interleukin (IL)-1ß, IL-6, CXCL1/KC, IL-10, tumor necrosis factor α, and transforming growth factor ß levels in BAL, collagen content in lung parenchyma, 5-HT levels in BAL fluid and in serum, the expression of 5-HT2B receptor, and Akt phosphorylation in lung tissue. RESULTS: AT reduced bleomycin-increased number of total cells (P < 0.001), neutrophils (P < 0.01), macrophages (P < 0.01), and lymphocytes (P < 0.05) in BAL. It also reduced the levels of IL-1ß (P < 0.01), IL-6 (P < 0.05), CXCL1/KC (P < 0.001), tumor necrosis factor α (P < 0.001), and transforming growth factor ß (P < 0.001). It increased expression of ant-inflammatory cytokine IL-10 (P < 0.001). It reduced bleomycin-increased 5-HT levels in BAL (P < 0.001) and in serum (P < 0.05). Reductions in collagen fiber deposition (P < 0.01), 5-HT2B receptor expression (P < 0.01), and Akt phosphorylation in lung tissue were observed. CONCLUSIONS: AT accelerates the resolution of lung inflammation and fibrosis in a model of bleomycin-induced lung fibrosis partly via attenuation of 5-HT/Akt signaling.
