2M高速信令链路MTP2的分析与设计

随着全国电信业务量的不断增加，特别是移动用户数量的剧增，原有的No．7信令网中使用的信令链路的带宽已经不能完全适应网上业务量的需求，无论是电信运营部门还是设备生产厂商都提出了对高速信令链路的需求；另一方面由于芯片技术的发展，微处理器速度的不断提升也为实现高速信令链路在技术上提供了支持。分析了2M高速信令链路与No．7信令链路在协议上的差别以及2M高速信令链路在MTP2层的软件设计以及功能划分，从而为具体实现提供了步骤及方法。     

无线Ad Hoc网络支持QoS的研究进展与展望

无线ad hoc网络的应用环境以及与Internet的互连要求它必须提供一定的服务质量(QoS)保证,然而,无线信道固有的特点及节点移动造成网络拓扑的频繁变化,使得在无线ad hoc网络中支持QoS面临许多新的挑战.从无线ad hoc网络的QoS体系结构、QoS路由、QoS信令、支持业务区分和资源预留的介质访问控制协议这4个方面出发,对近年来国内外在该方向取得的研究成果作了全面的概括总结和比较分析,系统阐述了在无线ad hoc网络中支持QoS的问题,指出了亟待解决的问题和今后的研究方向.     

三峡枢纽梯级调度交换网的组建

三峡枢纽梯级调度交换网由3种机型、6套交换机、10多部调度台，多种信令接口方式组成。担负着国调至三峡梯调，三峡梯调至三峡左岸电站，三峡梯调至葛洲坝大江电厂和二江电厂，三峡船闸至枢纽等有关单位的调度通信。文中以组网方式及信令接口为主，介绍三峡枢纽梯级调度交换网的特点及信令接口。     

The PKR/P38/RIPK1 Signaling Pathway as a Therapeutic Target in Alzheimer’s Disease

Neuropathological lesions in Alzheimer’s disease (AD) include amyloid plaques formed by the accumulation of amyloid peptides, neurofibrillary tangles made of hyperphosphorylated tau protein, synaptic and neuronal degenerations, and neuroinflammation. The cause of AD is unknown, but according to the amyloid hypothesis, amyloid oligomers could lead to the activation of kinases such as eukaryotic translation initiation factor 2-alpha kinase 2 (PKR), p38, and receptor-interacting serine/threonine-protein kinase 1 (RIPK1), which all belong to the same stress-activated pathway. Many toxic kinase activations have been described in AD patients and in experimental models. A p38 mitogen-activated protein kinase inhibitor was recently tested in clinical trials but with unsuccessful results. The complex PKR/P38/RIPK1 (PKR/dual specificity mitogen-activated protein kinase kinase 6 (MKK6)/P38/MAP kinase-activated protein kinase 2 (MK2)/RIPK1) is highly activated in AD brains and in the brains of AD transgenic animals. To delineate the implication of this pathway in AD, we carried out a search on PubMed including PKR/MKK6/p38/MK2/RIPK1, Alzheimer, and therapeutics. The involvement of this signaling pathway in the genesis of AD lesions, including Aβ accumulations and tau phosphorylation as well as cognitive decline, is demonstrated by the reports described in this review. A future combination strategy with kinase inhibitors should be envisaged to modulate the consequences for neurons and other brain cells linked to the abnormal activation of this pathway.     

Crossing Paths in Human Renal Cell Carcinoma (hRCC)

Historically, cell-signaling pathways have been studied as the compilation of isolated elements into a unique cascade that transmits extracellular stimuli to the tumor cell nucleus. Today, growing evidence supports the fact that intracellular drivers of tumor progression do not flow in a single linear pathway, but disseminate into multiple intracellular pathways. An improved understanding of the complexity of cancer depends on the elucidation of the underlying regulatory networks at the cellular and intercellular levels and in their temporal dimension. The high complexity of the intracellular cascades causes the complete inhibition of the growth of one tumor cell to be very unlikely, except in cases in which the so-called “oncogene addiction” is known to be a clear trigger for tumor catastrophe, such as in the case of gastrointestinal stromal tumors or chronic myeloid leukemia. In other words, the separation and isolation of the driver from the passengers is required to improve accuracy in cancer treatment. This review will summarize the signaling pathway crossroads that govern renal cell carcinoma proliferation and the emerging understanding of how these pathways facilitate tumor escape. We outline the available evidence supporting the putative links between different signaling pathways and how they may influence tumor proliferation, differentiation, apoptosis, angiogenesis, metabolism and invasiveness. The conclusion is that tumor cells may generate their own crossroads/crosstalk among signaling pathways, thereby reducing their dependence on stimulation of their physiologic pathways.     

Examining the Signaling Effect of E-tailers’ Return Policies

E-tailers normally have more accurate information regarding their products and services than consumers due to the nature of online transactions. To reduce consumers’ concerns of hidden information, e-tailers can use lenient return policies to attempt to signal high product and service quality. This research proposes a model to investigate the signaling effect of two components of return policy, return window—short return window vs. long return window and return depth—full refund vs. partial refund, on product quality and service quality. Data was collected using an online survey and analyzed using structural equation modeling. The results show that both a long return window and a full refund signal high service quality, which then positively affects purchase intention. When it comes to product quality, return window does not have a signaling effect, while the signaling effect of return depth is moderated by service quality.     

3-<i>epi</i>-bufotalin suppresses the proliferation in colorectal cancer cells through the inhibition of the JAK1/STAT3 signaling pathway

Traditional Chinese medicine (TCM) has been increasingly employed in the last decades in China for both preventing and treating a variety of cancers. 3-epi-bufotalin is an active ingredient of TCM “Chanpi” with anti-tumor potential. However, the effect and mechanism of 3-epi-bufotalin on colorectal cancers were not well disclosed. The present study demonstrated that 3-epi-bufotalin could reduce viability, trigger apoptosis, and block the cell cycle at the G₂/M stage in colorectal cancer cell lines HT29, RKO, and COLO205 in vitro. Moreover, 3-epi-bufotalin inhibited the JAK1/STAT3 signaling pathway. These results indicated the anti-proliferation ability of 3-epi-bufotalin in colorectal cancer cells.     

The Role of Cholesterol on Triterpenoid Saponin-Induced Endolysosomal Escape of a Saporin-Based Immunotoxin

Cholesterol seems to play a central role in the augmentation of saporin-based immunotoxin (IT) cytotoxicity by triterpenoid saponins. Endolysosomal escape has been proposed as one mechanism for the saponin-mediated enhancement of targeted toxins. We investigated the effects of lipid depletion followed by repletion on Saponinum album (SA)-induced endolysosomal escape of Alexa Fluor labelled saporin and the saporin-based immunotoxin OKT10-SAP, directed against CD38, in Daudi lymphoma cells. Lipid deprived cells showed reduced SA-induced endolysosomal escape at two concentrations of SA, as determined by a flow cytometric method. The repletion of membrane cholesterol by low density lipoprotein (LDL) restored SA-induced endolysosomal escape at a concentration of 5 µg/mL SA but not at 1 µg/mL SA. When LDL was used to restore the cholesterol levels in lipid deprived cells, the SA augmentation of OKT10-SAP cytotoxicity was partially restored at 1 µg/mL SA and fully restored at 5 µg/mL SA. These results suggest that different mechanisms of action might be involved for the two different concentrations of SA and that endosomal escape may not be the main mechanism for the augmentation of saporin IT cytotoxicity by SA at the sub-lytic concentration of 1 µg/mL SA.     

Interaction of IL-22/IL-22R1 promotes cell proliferation and suppresses apoptosis of colorectal cancer via phosphorylation of STAT3

Interleukin-22 (IL-22) is a member of IL-10 cytokine family which is expressed in activated T cells predominantly and in activated natural killer cells at lower levels. Previous studies have demonstrated the link between elevated levels of IL-22 and disease severity of psoriasis, Crohn’s disease, rheumatoid arthritis and interstitial lung diseases. However, the function of IL-22 in the development and progression of colorectal cancer (CRC) remains elusive. In this study, we first evaluated the IL-22/IL-22R1 level in CRC patients, and found that tumor tissues have more active expression of IL-22 and IL-22R1 than normal tissues, presenting correlation with the degree of differentiation of tumor tissues. Subsequently, Caspase and cell viability assays were performed on SW-480 cell line which expresses high level of IL-22R1 to examine if the supplementation of IL-22 has an impact on apoptosis and proliferation. In comparison with treatment of 5-FU, supplementation of IL-22 promoted cell proliferation and ameliorated apoptosis. To unveil signal transduction upon activation of IL-22R, we examined the phosphorylation of STAT3 in SW-480 cell line following supplementation of IL-22. The treatment of IL-22 also increased the level of p-Akt, an essential component in PI3K/Akt pathway. Although the link between STAT3 phosphorylation and PI3K/ Akt activation remains to be explored, our study revealed the mechanism underlying the effects of IL-22R activation on apoptosis as well as tumor differentiation, indicating the prognostic value of IL-22/IL-22R.