WCDMA系统接口信令消息的描述与实现

WCDMA作为第三代移动通信系统的主流标准，能够提供多种类型的多媒体服务。为了实现各种用户平面数据的传输，系统会提前通过控制平面对所需的无线资源进行分配。由于配置过程是通过接口之间发送控制平面应用协议消息来实现的，因此能否正确有效地对信令消息进行编解码成为保证系统稳定工作的关键因素。3GPP标准中，ASN．1语言被用来描述接口信令消息。首先简要介绍了WCDMA系统结构以及主要接口协议，重点描述了ASN．1存在的意义及其编解码规则，最后给出了基于ASN．1的开发环境下应用层网络协议的开发流程。     

自动交换光网络的信令控制方式研究

自动交换光网络是一种能够自动完成网络连接的新型网络。他由控制面、传送面和管理面3个平面组成，控制面技术是其核心，利用控制面能够实施动态交换。本文在研究分析已有的光网络信令控制方式的基础上，提出了一种混合信令控制方式，他具有更好的性能和信令控制能力，适合ASON的信令网和控制面要求。     

下一代网络--多协议标记交换MPLS思想剖析

多协议标记交换MPLS通过在传统的IP包里加入标记，使原来依赖于IP头标分析的路由转发转变为依赖于标记的转发，这不仅可以大大地提高IP包的转发速度，更可使传统IP网络具有QoS能力。本文深入分析了标记转发的思想．并指出了MPLS实现其优点所用的机制与原理。     

铁路信号电缆断线故障在线监测与定位方法研究

铁路信号电缆是保证列车安全运营的重要组成部分,其故障严重影响列车的安全运营;由于其经多个分线盒接线柱连接的敷设特点,存在中间接头过多,致使传统的电缆故障检测方法应用受到了极大的限制;为此,通过在电缆中间分线盒的备用芯线对接线柱中接入固定阻值的电阻,将备用芯线对形成闭合回路网络,然后在线监测其电阻阻值,利用回路阻值的变化来反映电缆状态,并以在线监测备用芯线对代替在用芯线对,进而在不影响正常列控信号传输的情况下实现了信号电缆的故障在线监测;经实际测试,有效地解决了铁路信号电缆断线故障的在线监测及定位。     

Intracellular Ca2+ Signaling in Protozoan Parasites: An Overview with a Focus on Mitochondria

Ca²⁺ signaling has been involved in controling critical cellular functions such as activation of proteases, cell death, and cell cycle control. The endoplasmatic reticulum plays a significant role in Ca²⁺ storage inside the cell, but mitochondria have long been recognized as a fundamental Ca²⁺ pool. Protozoan parasites such as Plasmodium falciparum, Toxoplasma gondii, and Trypanosoma cruzi display a Ca²⁺ signaling toolkit with similarities to higher eukaryotes, including the participation of mitochondria in Ca²⁺-dependent signaling events. This review summarizes the most recent knowledge in mitochondrial Ca²⁺ signaling in protozoan parasites, focusing on the mechanism involved in mitochondrial Ca²⁺ uptake by pathogenic protists.     

Current Understandings on Magnesium Deficiency and Future Outlooks for Sustainable Agriculture

The productivity of agricultural produce is fairly dependent on the availability of nutrients and efficient use. Magnesium (Mg²⁺) is an essential macronutrient of living cells and is the second most prevalent free divalent cation in plants. Mg²⁺ plays a role in several physiological processes that support plant growth and development. However, it has been largely forgotten in fertilization management strategies to increase crop production, which leads to severe reductions in plant growth and yield. In this review, we discuss how the Mg²⁺ shortage induces several responses in plants at different levels: morphological, physiological, biochemical and molecular. Additionally, the Mg²⁺ uptake and transport mechanisms in different cellular organelles and the role of Mg²⁺ transporters in regulating Mg²⁺ homeostasis are also discussed. Overall, in this review, we critically summarize the available information about the responses of Mg deficiency on plant growth and development, which would facilitate plant scientists to create Mg²⁺-deficiency-resilient crops through agronomic and genetic biofortification.     

Modulation of Tubular pH by Acetazolamide in a Ca2+ Transport Deficient Mice Facilitates Calcium Nephrolithiasis

Proximal tubular (PT) acidosis, which alkalinizes the urinary filtrate, together with Ca²⁺ supersaturation in PT can induce luminal calcium phosphate (CaP) crystal formation. While such CaP crystals are known to act as a nidus for CaP/calcium oxalate (CaOx) mixed stone formation, the regulation of PT luminal Ca²⁺ concentration ([Ca²⁺]) under elevated pH and/or high [Ca²⁺] conditions are unknown. Since we found that transient receptor potential canonical 3 (TRPC3) knockout (KO; -/-) mice could produce mild hypercalciuria with CaP urine crystals, we alkalinized the tubular pH in TRPC3-/- mice by oral acetazolamide (0.08%) to develop mixed urinary crystals akin to clinical signs of calcium nephrolithiasis (CaNL). Our ratiometric (λ340/380) intracellular [Ca²⁺] measurements reveal that such alkalization not only upsurges Ca²⁺ influx into PT cells, but the mode of Ca²⁺ entry switches from receptor-operated to store-operated pathway. Electrophysiological experiments show enhanced bicarbonate related current activity in treated PT cells which may determine the stone-forming phenotypes (CaP or CaP/CaOx). Moreover, such alkalization promotes reactive oxygen species generation, and upregulation of calcification, inflammation, fibrosis, and apoptosis in PT cells, which were exacerbated in absence of TRPC3. Altogether, the pH-induced alteration of the Ca²⁺ signaling signature in PT cells from TRPC3 ablated mice exacerbated the pathophysiology of mixed urinary stone formation, which may aid in uncovering the downstream mechanism of CaNL.     

The GNAQ T96S Mutation Affects Cell Signaling and Enhances the Oncogenic Properties of Hepatocellular Carcinoma

Hepatocellular carcinoma (HCC), the most common malignant tumor in the liver, grows and metastasizes rapidly. Despite advances in treatment modalities, the five-year survival rate of HCC remains less than 30%. We sought genetic mutations that may affect the oncogenic properties of HCC, using The Cancer Genome Atlas (TCGA) data analysis. We found that the GNAQ T96S mutation (threonine 96 to serine alteration of the Gαq protein) was present in 12 out of 373 HCC patients (3.2%). To examine the effect of the GNAQ T96S mutation on HCC, we transfected the SK-Hep-1 cell line with the wild-type or the mutant GNAQ T96S expression vector. Transfection with the wild-type GNAQ expression vector enhanced anchorage-independent growth, migration, and the MAPK pathways in the SK-Hep-1 cells compared to control vector transfection. Moreover, cell proliferation, anchorage-independent growth, migration, and the MAPK pathways were further enhanced in the SK-Hep-1 cells transfected with the GNAQ T96S expression vector compared to the wild-type GNAQ-transfected cells. In silico structural analysis shows that the substitution of the GNAQ amino acid threonine 96 with a serine may destabilize the interaction between the regulator of G protein signaling (RGS) protein and GNAQ. This may reduce the inhibitory effect of RGS on GNAQ signaling, enhancing the GNAQ signaling pathway. Single nucleotide polymorphism (SNP) genotyping analysis for Korean HCC patients shows that the GNAQ T96S mutation was found in only one of the 456 patients (0.22%). Our data suggest that the GNAQ T96S hotspot mutation may play an oncogenic role in HCC by potentiating the GNAQ signal transduction pathway.