Voice over IP

The area that this thesis covers is Voice over IP (or IP Telephony as it is sometimes called) over Private networks and not over the Internet. There is a distinction to be made between the two even though the term is loosely applied to both. IP Telephony over Private Networks involve calls made over private WANs using IP telephony protocols while IP Telephony over the Internet involve calls made over the public Internet using IP telephony protocols. Since the network is private, service is reliable because the network owner can control how resources are allocated to various applications, such as telephony services. The public Internet on the other hand is a public, largely unmanaged network that offers no reliable service guarantee. Calls placed over the Internet can be low in quality, but given the low price, some find this solution attractive. What started off as an Internet Revolution with free phone calls being offered to the general public using their multimedia computers has turned into a telecommunication revolution where enterprises are beginning to converge their data and voice networks into one network. In retrospect, an enterprise\u27s data networks are being leveraged for telephony. The communication industry has come full circle. Earlier in the decade data was being transmitted over the public voice networks and now voice is just another application which is/will be run over the enterprises existing data networks. We shall see in this thesis the problems that are encountered while sending Voice over Data networks using the underlying IP Protocol and the corrective steps taken by the Industry to resolve these multitudes of issues. Paul M. Zam who is collaborating in this Joint Thesis/project on VoIP will substantiate this theoretical research with his practical findings. On reading this paper the reader will gain an insight in the issues revolving the implementation of VoIP in an enterprises private network as well the technical data, which sheds more light on the same. Thus the premise of this joint thesis/project is to analyze the current status of the technology and present a business case scenario where an organization will be able to use this information

Rapid light-induced activation of retinal microglia in mice lacking Arrestin-1

Microglia dynamically prune synaptic contacts during development, and digest waste that accumulates in degeneration and aging. In many neurodegenerative diseases, microglial activation and phagocytosis gradually increase over months or years, with poorly defined initial triggering events. Here, we describe rapid retinal microglial activation in response to physiological light levels in a mouse model of photoreceptor degeneration that arises from defective rhodopsin deactivation and prolonged signaling. Activation, migration and proliferation of microglia proceeded along a well-defined time course apparent within 12 h of light onset. Retinal imaging in vivo with optical coherence tomography revealed dramatic increases in light-scattering from photoreceptors prior to the outer nuclear layer thinning classically used as a measure of retinal neurodegeneration. This model is valuable for mechanistic studies of microglial activation in a well-defined and optically accessible neural circuit, and for the development of novel methods for detecting early signs of pending neurodegeneration in vivo

MicroRNA signatures and Foxp3+ cell count correlate with relapse occurrence in follicular lymphoma

First line drug treatment of follicular lymphoma (FL) patients is followed by a highly variable disease-free time before relapse in about one third of patients. No molecular marker is able to predict efficiently the risk of relapse. We investigated the expression profile of microRNAs (miRNAs) by microarrays and of the tumor microenvironment by immunohistochemistry in 26 FLs and 12 reactive lymph nodes (rLN) as reference. Twenty-nine miRNAs were differentially expressed in FLs compared to rLNs and some of them discriminated grade 1 from 3a FLs. Both FLs and rLNs displayed molecular heterogeneity. FLs grouped into two clusters mostly driven by the tumor T-cell content. Among 21 drug-treated FL patients with an average follow-up of 13.5 years, eight cases relapsed. Twenty-six miRNAs discriminated between relapsed and non-relapsed FLs. Ten miRNAs also correlated with Foxp3+ cells number. Notably, Foxp3+ cells were significantly less in relapsed patients and lower Foxp3+ cell number associated with shorter time-to-relapse. Foxp3+ cells did not co-expressed follicular helper T-cell markers and were therefore classified as regulatory T cells rather than follicular regulatory T-cells. These findings introduce new knowledge about the relationship between miRNA alterations and infiltrating immune cells and show that Foxp3+ cells might be predictive of disease relapse

MYC-related microRNAs signatures in non-Hodgkin B-cell lymphomas and their relationships with core cellular pathways

In order to investigate the role of microRNAs in the pathogenesis of different B-cell lymhoma subtypes, we have applied an array-based assay to a series of 76 mixed non-Hodgkin B-cell lymphomas, including Burkitt's lymphoma (BL), diffuse large B-cell lymphoma, primary mediastinal B-cell lymphoma, mantle cell lymphoma (MCL) and follicular lymphoma. Lymphomas clustered according to histological subtypes, driven by two miRNA clusters (the miR-29 family and the miR-17-92 cluster). Since the two miRNA clusters are known to be MYC-regulated, we investigated whether this would be supported in MYC-driven experimental models, and found that this signature separated BL cell lines and a MYC-translocated MCL cell lines from normal germinal center B-cells and other B-cell populations. Similar results were also reproduced in tissue samples comparing BL and reactive lymph node samples. The same series was then quantitatively analyzed for MYC expression by immunohistochemistry and MYC protein levels were compared with corresponding miRNA signatures. A specific metric was developed to summarize the levels of MYC-related microRNAs and the corresponding protein levels. We found that MYC-related signatures are directly related to MYC protein expression across the whole spectrum of B-cells and B-cell lymphoma, suggesting that the MYC-responsive machinery shows predominantly quantitative, rather than qualitative, modifications in B-cell lymphoma. Novel MYC-related miRNAs were also discovered by this approach. Finally, network analysis found that in BL MYC-related differentially expressed miRNAs could control, either positively or negatively, a limited number of hub proteins, including BCL2, CDK6, MYB, ZEB1, CTNNB1, BAX and XBP1