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This research analyzed the real-world NOx and particle number (PN) emissions of 21 China VI heavy-duty diesel trucks (HDDTs). On-road emission conformity was first evaluated with portable emission measurement system (PEMS). Only 76.19 %, 71.43 % and 61.90 % of the vehicles passed the NOx test, PN test and both tests, respectively. The impacts of vehicle features including exhaust gas recirculation (EGR) equipment, mileage and tractive tonnage were then assessed. Results demonstrated that EGR helped reducing NOx emission factors (EFs) while increased PN EFs. Larger mileages and tractive tonnages corresponded to higher NOx and PN EFs, respectively. In-depth analyses regarding the influences of operating conditions on emissions were conducted with both numerical comparisons and statistical tests. Results proved that HDDTs generated higher NOx EFs under low speeds or large vehicle specific powers (VSPs), and higher PN EFs under high speeds or small VSPs in general. In addition, unqualified vehicles generated significantly higher NOx EFs than qualified vehicles on freeways or under speed≥40 km/h, while significant higher PN EFs were generated on suburban roads, freeways or under operating modes with positive VSPs by unqualified vehicles. The reliability and accuracy of on-board diagnostic (OBD) NOx data were finally investigated. Results revealed that 43 % of the test vehicles did not report reliable OBD data. Correlation analyses between OBD NOx and PEMS measurements further demonstrated that the consistency of instantaneous concentrations were generally low. However, sliding window averaged concentrations show better correlations, e.g., the Pearson correlation coefficients on 20s-window averaged concentrations exceeded 0.85 for most vehicles. The research results provide valuable insights into emission regulation, e.g., focusing more on medium- to high-speed operations to identify unqualified vehicles, setting higher standards to improve the quality of OBD data, and adopting window averaged OBD NOx concentrations in evaluating vehicle emission performance. 

Abstract SARS-CoV-2 infection causes spike-dependent fusion of infected cells with ACE2 positive neighboring cells, generating multi-nuclear syncytia that are often associated with severe COVID. To better elucidate the mechanism of spike-induced syncytium formation, we combine chemical genetics with 4D confocal imaging to establish the cell surface heparan sulfate (HS) as a critical stimulator for spike-induced cell-cell fusion. We show that HS binds spike and promotes spike-induced ACE2 clustering, forming synapse-like cell-cell contacts that facilitate fusion pore formation between ACE2-expresing and spike-transfected human cells. Chemical or genetic inhibition of HS mitigates ACE2 clustering, and thus, syncytium formation, whereas in a cell-free system comprising purified HS and lipid-anchored ACE2, HS stimulates ACE2 clustering directly in the presence of spike. Furthermore, HS-stimulated syncytium formation and receptor clustering require a conserved ACE2 linker distal from the spike-binding site. Importantly, the cell fusion-boosting function of HS can be targeted by an investigational HS-binding drug, which reduces syncytium formation in vitro and viral infection in mice. Thus, HS, as a host factor exploited by SARS-CoV-2 to facilitate receptor clustering and a stimulator of infection-associated syncytium formation, may be a promising therapeutic target for severe COVID.