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Classical transportation systems have been suffering from inefficiency in utilizing road capacity and incapability of guaranteeing safety due to inconsistent and unpredictable human based manipulations. This long standing issue is expected to be resolved through the introduction of vehicular autonomy, along with a properly configured traffic management system and an underlying communication network that supports the dissemination of safety and control messages. However, mechanisms to be used in the regulation of autonomous vehicles are yet to be developed.For the first part of the dissertation, we propose an efficient data dissemination protocol, identified as Vehicular Backbone Network (VBN), which support high throughput and low delay message delivery across a Vehicular Ad Hoc Network (VANET). Vehicles are elected as relay nodes at properly selected nominal positions to optimize system throughput rate with guaranteed outage probability. The proposed VBN mechanism is analyzed under different Medium Access Control (MAC) protocols and various stochastic traffic flow conditions.In the second part of the dissertation, we go beyond the statistical vehicular traffic modeland present our study of a platoon-based autonomous vehicular traffic regulation system. The traffic management system, serving to configure vehicles into platoons and regulating the on-ramp access of vehicular flows into the highway, is integrated with a design of a VANET system. The latter provides for the communications of essential message flows among highway vehicles. The fundamental tradeoffs that need to be made in designing the autonomous systems are modeled and studied. We propose an optimization framework to be used in designing the traffic control system in a manner that meet throughput and latency performance metrics across the vehicular mobility and the message communications networking dimensions of the overall system. We also study the design of a core network that employs Road Side Units (RSUs) that provide communications networking support in disseminating message flows to/from and among highway vehicles.

To investigate whether microRNA (miRNA) miR-21 regulates dimethylarginine dimethylaminohydrolase 1 (DDAH1) expression through binding 3'-UTR region directly in human umbilical venous endothelial cells (HUVECs) and to explore whether DDAH1-V2/V3 transcripts can function as microRNA sponge, thereby modulating DDAH1-V1 expression.The DDAH1 3'-UTR containing miR-21 recognizing sequence was cloned into PmirGLO dual-luciferase miRNA target expression plasmid to construct PmirGLO-miR-21. The plasmid and miR-21 (at concentrations of 25, 50, 100 nM, respectively) or negative control (100 nM) were co-transfected into HUVECs, luciferase activity was detected at 24 h. HUVECs were incubated with 2 μg/ml Actinomycin D for the indicated time after miR-21 (25 nM) transfection, half-lives of DDAH1 mRNA were determined. HUVECs were transfected with PmirGLO-miR-21 alone or co-transfected with miR-21 for 24 h, DDAH1 transcripts mRNA, eNOS activity and DDAH1 protein expression were determined.MiR-21 decreased luciferase activity of PmirGLO-miR-21 in a dose-dependent manner (P 0.05 for 25 nM miR-21, P 0.01 for 50 nM and 100 nM miR-21), and miR-21 inhibitor increased reporter activity of PmirGLO-miR-21 and mRNA expression of all three DDAH1 transcript variants significantly (P 0.05, respectively). The degree of increase in endogenous DDAH1 mRNA expression by miR-21 inhibitor was more obvious for DDAH1-V3. Overexpression of miR-21 decreased mRNA expression and mRNA half-life time of all DDAH1 transcripts significantly (P 0.05), and DDAH1-V2 displayed significantly decreased half-life time than DDAH1-V1 and -V3 with or without miR-21 transfection (P 0.05, respectively). MiR-21 (100 nM) decreased DDAH1 protein expression and eNOS activity significantly (P 0.05), which was reversed by PmirGLO-miR-21 transfection (P 0.05). Transfection of PmirGLO-miR-21 alone increased intracellular miR-21 expression by approximately 5.6-fold, but only showed a trend of increase in DDAH1 protein expression.Our results confirmed DDAH1 3'-UTR as a target for miR-21, and endogenous miR-21 showed increased inhibitory effect on DDAH1-V3 transcript. DDAH1 3'-UTR, especially for DDAH1-V3, may function as miR-21 sponge to regulate DDAH1 protein expression. Modulation of miR-21-DDAH1 interaction may provide a new approach for tackling cardiovascular diseases.

Profiling of both the genome and the transcriptome promises a comprehensive, functional readout of a tissue sample, yet analytical approaches are required to translate the increased data dimensionality, heterogeneity and complexity into patient benefits. We developed a statistical approach called Texomer ( https://github.com/KChen-lab/Texomer ) that performs allele-specific, tumor-deconvoluted transcriptome-exome integration of autologous bulk whole-exome and transcriptome sequencing data. Texomer results in substantially improved accuracy in sample categorization and functional variant prioritization.

Background: Colorectal cancer (CRC) represents the third most common type of cancer and the third leading cause of death from cancer around the world. M701 is a CD3/EpCAM bispecific antibody that shows promising cytotoxicity toward CRC cells. Aim: To investigate the influence of immuno-related gene polymorphisms on M701 mediated cytotoxicity to CRC cell HCT116. Method: We analyzed the influence of the effect of M701 on the activation and cytotoxicity of peripheral mononuclear blood cells from 129 healthy volunteers with different genotypes. Result: When incubated with M701, peripheral mononuclear blood cells from CD247 rs2949655 AA homozygotes showed significantly lower cytotoxicity than those from AG/GG heterozygotes. Conclusion: CD247 rs2949655 was significantly associated with the cytotoxicity of M701 to HCT116, which might contribute to personalized medicine of M701.