The track finding algorithm of the Belle II vertex detectors

The Belle II experiment is a high energy multi purpose particle detector operated at the asymmetric e+e-- collier SuperKEKB in Tsukuba (Japan). In this work we describe the algorithm performing the pattern recognition for inner tracking detector which consists of two layers of pixel detectors and four layers of double sided silicon strip detectors arranged around the interaction region. The track finding algorithm will be used both during the High Level Trigger on-line track reconstruction and during the off-line full reconstruction. It must provide good efficiency down to momenta as low as 50 MeV/c where material effects are sizeable even in an extremely thin detector as the VXD. In addition it has to be able to cope with the high occupancy of the Belle II detectors due to the background. The underlying concept of the track finding algorithm, as well as details of the implementation are outlined. The algorithm is proven to run with good performance on simulated Y (4S) â\u86\u92 BB events with an efficiency for reconstructing tracks of above 90% over a wide range of momentum

“Genes”

In order to describe a cell at molecular level, a notion of a “gene” is neither necessary nor helpful. It is sufficient to consider the molecules (i.e., chromosomes, transcripts, proteins) and their interactions to describe cellular processes. The downside of the resulting high resolution is that it becomes very tedious to address features on the organismal and phenotypic levels with a language based on molecular terms. Looking for the missing link between biological disciplines dealing with different levels of biological organization, we suggest to return to the original intent behind the term “gene”. To this end, we propose to investigate whether a useful notion of “gene” can be constructed based on an underlying notion of function, and whether this can serve as the necessary link and embed the various distinct gene concepts of biological (sub)disciplines in a coherent theoretical framework. In reply to the Genon Theory recently put forward by Klaus Scherrer and Jürgen Jost in this journal, we shall discuss a general approach to assess a gene definition that should then be tested for its expressiveness and potential cross-disciplinary relevance

Status of the BELLE II Pixel Detector

The Belle II experiment at the super KEK B-factory (SuperKEKB) in Tsukuba, Japan, has been collecting $e^+e^−$ collision data since March 2019. Operating at a record-breaking luminosity of up to $4.7×10^{34} cm^{−2}s^{−1}$, data corresponding to $424 fb^{−1}$ has since been recorded. The Belle II VerteX Detector (VXD) is central to the Belle II detector and its physics program and plays a crucial role in reconstructing precise primary and decay vertices. It consists of the outer 4-layer Silicon Vertex Detector (SVD) using double sided silicon strips and the inner two-layer PiXel Detector (PXD) based on the Depleted P-channel Field Effect Transistor (DePFET) technology. The PXD DePFET structure combines signal generation and amplification within pixels with a minimum pitch of $(50×55) μm^2$. A high gain and a high signal-to-noise ratio allow thinning the pixels to $75 μm$ while retaining a high pixel hit efficiency of about $99$. As a consequence, also the material budget of the full detector is kept low at $≈0.21$$\frac{X}{X_0}$ per layer in the acceptance region. This also includes contributions from the control, Analog-to-Digital Converter (ADC), and data processing Application Specific Integrated Circuits (ASICs) as well as from cooling and support structures. This article will present the experience gained from four years of operating PXD; the first full scale detector employing the DePFET technology in High Energy Physics. Overall, the PXD has met the expectations. Operating in the intense SuperKEKB environment poses many challenges that will also be discussed. The current PXD system remains incomplete with only 20 out of 40 modules having been installed. A full replacement has been constructed and is currently in its final testing stage before it will be installed into Belle II during the ongoing long shutdown that will last throughout 2023

Research and Design of a Routing Protocol in Large-Scale Wireless Sensor Networks

无线传感器网络，作为全球未来十大技术之一，集成了传感器技术、嵌入式计算技术、分布式信息处理和自组织网技术，可实时感知、采集、处理、传输网络分布区域内的各种信息数据，在军事国防、生物医疗、环境监测、抢险救灾、防恐反恐、危险区域远程控制等领域具有十分广阔的应用前景。 本文研究分析了无线传感器网络的已有路由协议，并针对大规模的无线传感器网络设计了一种树状路由协议，它根据节点地址信息来形成路由，从而简化了复杂繁冗的路由表查找和维护，节省了不必要的开销，提高了路由效率，实现了快速有效的数据传输。 为支持此路由协议本文提出了一种自适应动态地址分配算——ADAR（AdaptiveDynamicAddre...As one of the ten high technologies in the future, wireless sensor network, which is the integration of micro-sensors, embedded computing, modern network and Ad Hoc technologies, can apperceive, collect, process and transmit various information data within the region. It can be used in military defense, biomedical, environmental monitoring, disaster relief, counter-terrorism, remote control of haz...学位：工学硕士院系专业：信息科学与技术学院通信工程系_通信与信息系统学号：2332007115216

Epstein-Barr virus–specific cytokine-induced killer cells for treatment of Epstein-Barr virus–related malignant lymphoma

Background: Prolonged immunosuppression or delayed T-cell recovery may favor Epstein-Barr virus (EBV) infection or reactivation after allogeneic hematopoietic stem cell transplantation (HSCT), which can lead to post-transplant lymphoproliferative disease (PTLD) and high-grade malignant B-cell lymphoma. Cytokine-induced killer (CIK) cells with dual specific anti-tumor and virus-specific cellular immunity may be applied in this context. Methods: CIK cells with EBV-specificity were generated from peripheral blood mononuclear cells (PBMCs), expanded in the presence of interferon-γ, anti-CD3, interleukin (IL)-2 and IL-15 and were pulsed twice with EBV consensus peptide pool. CIK cells with EBV-specificity and conventional CIK cells were phenotypically and functionally analyzed. Additionally, CIK cells with EBV-specificity were applied to a patient with EBV-related PTLD rapidly progressing to highly aggressive B-cell lymphoma on a compassionate use basis after approval and agreement by the regulatory authorities. Results: Pre-clinical analysis showed that generation of CIK cells with EBV-specificity was feasible. In vitro cytotoxicity analyses showed increased lysis of EBV-positive target cells, enhanced proliferative capacity and increased secretion of cytolytic and proinflammatory cytokines in the presence of EBV peptide-displaying target cells. In addition, 1 week after infusion of CIK cells with EBV-specificity, the patient's highly aggressive B-cell lymphoma persistently disappeared. CIK cells with EBV-specificity remained detectable for up to 32 days after infusion and infusion did not result in acute toxicity. Discussion: The transfer of both anti-cancer potential and T-cell memory against EBV infection provided by EBV peptide-induced CIK cells might be considered a therapy for EBV-related PTLD

Dasatinib enhances tumor growth in gemcitabine-resistant orthotopic bladder cancer xenografts

Background: Systemic chemotherapy with gemcitabine and cisplatin is standard of care for patients with metastatic urothelial bladder cancer. However, resistance formation is common after initial response. The protein Src is known as a proto-oncogene, which is overexpressed in various human cancers. Since there are controversial reports about the role of Src in bladder cancer, we evaluated the efficacy of the Src kinase inhibitor dasatinib in the urothelial bladder cancer cell line RT112 and its gemcitabine-resistant sub-line RT112rGEMCI20 in vitro and in vivo. Methods: RT112 urothelial cancer cells were adapted to growth in the presence of 20 ng/ml gemcitabine (RT112rGEMCI20) by continuous cultivation at increasing drug concentrations. Cell viability was determined by MTT assay, cell growth kinetics were determined by cell count, protein levels were measured by western blot, and cell migration was evaluated by scratch assays. In vivo tumor growth was tested in a murine orthotopic xenograft model using bioluminescent imaging. Results: Dasatinib exerted similar effects on Src signaling in RT112 and RT112rGEMCI20 cells but RT112rGEMCI20 cells were less sensitive to dasatinib-induced anti-cancer effects (half maximal inhibitory concentration (IC50) of dasatinib in RT112 cells: 349.2 ± 67.2 nM; IC50 of dasatinib in RT112rGEMCI20 cells: 1081.1 ± 239.2 nM). Dasatinib inhibited migration of chemo-naive and gemcitabine-resistant cells. Most strikingly, dasatinib treatment reduced RT112 tumor growth and muscle invasion in orthotopic xenografts, while it was associated with increased size and muscle-invasive growth in RT112rGEMCI20 tumors. Conclusion: Dasatinib should be considered with care for the treatment of urothelial cancer, in particular for therapy-refractory cases.Medicine, Faculty ofOther UBCNon UBCUrologic Sciences, Department ofReviewedFacult