The present research presents procedures for exploitation of level sensitive latches in wire pipelining. The user gives a Steiner tree, having a signal source and set of destination or sinks, and the location in rectangular plane, capacitive load and required arrival time at each of the destinations. The user also defines a library of non-clocked (buffer) elements and clocked elements (flip-flop and latch), also known as synchronous elements. The first procedure performs concurrent repeater and synchronous element insertion in a bottom-up manner to find the minimum latency that may be achieved between the source and the destinations. The second procedure takes additional input (required latency) for each destination, derived from previous procedure, and finds the repeater and synchronous element assignments for all internal nodes of the Steiner tree, which minimize overall area used. These procedures utilize the latency and area advantages of latch based pipelining over flip-flop based pipelining. The second procedure suggests two methods to tackle the challenges that exist in a latch based design. The deferred delay padding technique is introduced, which removes the short path violations for latches with minimal extra cost.

IEEE 802.11-based wireless local area networks (WLANs) have been set up in many public places in last few years. It provides convenient network connectivity to mobile nodes (MNs) and allows users moving from one wireless network to another. With mobility protocol support, such as Mobile IPv6 (MIPv6), people can roam across wireless IP subnets without loss of network-layer connectivity. However, the handover latency may make users feel uncomfortable in MIPv6. To support seamless handover, an enhanced MIPv6 scheme, Fast Handovers for Mobile IPv6 (FMIPv6)[13], was been proposed. In order to further reduce the handover latency, integrating the lower layer procedure with the upper layer procedure is necessary. Unfortunately, when integrating the IEEE 802.11-based standard with FMIPv6, FMIPv6 always fails to perform predictive handover procedure. This may make the handover procedure result in reactive handover. It is because of the protocol nature of IEEE 802.11 and the weak relation between IEEE 802.11 and FMIPv6. Furthermore, a MN can¡¦t receive packets destined to it when it sends the Fast Binding Update (FBU) to the original access router (OAR). This would cause unnecessary packet loss and make the redictive handover have more packet loss then reactive. Those issues will cause quality of services degradation and make real-time applications unreachable. In this dissertation, a low-latency MIPv6 handover scheme will be proposed. It is a FMIPv6-based scheme which is assisted by an active-scan link layer scheme. It has the advantage of FMIPv6 and can reduce unnecessary packet loss when the handover occurs. Also, with the assistance of the active scheme, it can avoid the longest phase that IEEE 802.11 will enter, and can lower the handover latency.

Tor is a popular anonymity-preserving network, consisting of routers run by volunteers all around the world. It protects Internet users’ privacy by relaying their network traffic through a series of routers, thus concealing the linkage between the sender and the recipient. Despite the advantage of Tor’s anonymizing capabilities, it also brings extra latency, which discourages more users from joining the network. One of the factors that causes the latency lies in Tor’s circuit scheduling algorithm, which allows busy circuits to crowd out bursty circuits. In this work, we propose and implement a more advanced scheduling algorithm which treats circuits differently, based on their recent activity. In this way, bursty circuits such as those used for web browsing can gain higher priority over busy ones such as used for bulk transfer; the performance for most activities over Tor is improved, while minimal overhead is incurred. Our algorithm has been incorporated into the latest build of Tor.

Thesis (Ph. D.)--University of Washington, 2008. / Vita. Includes bibliographical references (p. 144-163).

The master thesis is dealing with Internet host localization methods, more exactly with determining geographical position of the unknown Internet host connected to the network using RTT delay measuring. The first part is dealing with description of RTT delays that may occur in the network and tools for their measurement. The next is part of thesis is devoted to description of two kinds of localization methods. Ones that are using existing data to determine the position of Internet host also called passive methods, and others that are using RTT delay measurement, also called active methods. The main part is focused on GeoWeight method which is based on geographical localization estimation of Internet host. It is based on RTT delay measurement using the principles of CBG method, enhanced by introduction of the theory of weights according to the probability of the target Internet host. The last part is describing the application that was made to determine the geographic localization of the target Internet host using GeoWeight method. The application was afterwards tested by measuring RTT delay in PlanetLab experimental network. At the end the final measured results were compared with other localization methods (CBG, Octant, SOI, GeoIP).

Audio perception latency can influence the performance ability of a musician. A phenomenographic study is conducted to discuss the issue of perception latency and determine the amount of latency musicians can tolerate. Potential contributing factors such as their musical training, studio experience, and ability to perform with a metronomic aid were taken into account. Upon completion of the performance aspect of the study, the researcher then conducted a semi-structured interview with each individual participant in which a series of questions were asked about the experiment. It is found that musicians employ various techniques to compensate for perception latency and that there is a maximum amount of latency that musicians can tolerate during a musical performance. Keywords: perception latency, reception latency, response latency, maximum latency, delay, optimal performance, tolerable performance. / Mini Dissertation (MMus)--University of Pretoria, 2016. / Music / MMus / Unrestricted

Le virus Herpes Simplex de type 1 (HSV1) est responsable chez l’homme, son seul hôte naturel, d’infections oculaires cornéennes (kératites) récurrentes, typiquement unilatérales, pouvant induire une perte majeure de la vision. Pendant toute la vie, le virus reste à l’état quiescent (latence) dans le système nerveux, en particulier dans les deux ganglions trigéminés (TG) qui sont responsables de l’innervation sensitive de la cornée. La réactivation du virus à partir de ces TG entraine la kératite. Jusqu’à présent, les seuls traitements disponibles contre HSV1 ne sont que curatifs, c’est à dire qu’ils permettent de contrôler la réactivation que lorsque est déclarée. Il n’existe pour l’instant aucune thérapeutique réellement préventive sur l’ensemble des récidives, en particulier aucun vaccin n’a fait la preuve de son efficacité.Notre équipe a caractérisé un modèle d’infection herpétique par primo-infection orale, qui reproduit chez la souris une grande partie de l’histoire naturelle de l’infection herpétique telle qu’elle est observée chez l’homme. Ce modèle reproduit aussi la latéralisation, puisque la kératite initiale (puis ses récidives éventuelles) n’est observée que du côté inoculé, alors que l’infection latente est retrouvée dans les deux TG. Cependant, cette latence bilatérale n’est pas parfaitement symétrique à l’échelle moléculaire: alors que la charge virale latente (nombre de copies de génome) est similaire entre les deux TG, la production de LAT (Latency-Associated Transcripts) est plus importante du côté inoculé, de même que le nombre de neurones exprimant ces LAT (Cavallero et al., 2014; Maillet et al., 2006). Or, l’expression des LAT, marqueur classique de l’infection latente par HSV1, est associée, d’après la littérature scientifique, à la possibilité ultérieure de réactivation virale. A l’inverse, une infection herpétique sans expression des LAT est considérée comme peu réactivable (Perng et al., 2000). L’asymétrie biologique observée dans notre modèle pourrait donc expliquer la plus forte capacité de réactivation de HSV1 du côté inoculé seulement.L’objectif de l’ensemble de notre projet a été de tenter de contraindre une souche virale sauvage (à virulence normale) à une infection latente mais à capacité réduite de réactivation (sans expression de LAT), c’est à dire comme observé du côté non-inoculé de notre modèle. Pour cela, nous avons étudié l’effet de la primo-infection herpétique d’une souche de HSV1 sur la sensibilité des tissus à héberger l’infection latente par une autre souche virale, inoculée ultérieurement et dans un autre site.Notre avons montré que la primo-infection par une souche de HSV1 a inhibé la pathogénie (morbidité et mortalité) induite une autre souche de HSV1 virulente, inoculée quelques jours après. La primo-infection a contraint cette souche réinfectante à une mise en latence sans réplication au préalable, cette latence ne s’accompagnant pas d’expression de LAT. Cet effet inhibiteur a également été observé lors de l’utilisation d’une souche atténuée, non virulente dans le système nerveux, lors de la primo-infection. L’étude de la réactivation des différentes souches a révélé que lors de l’utilisation d’une souche neurovirulente et réactivable en tant que souche de primo-infection, la souche réinfectante pouvait également réactiver (aussi bien que son contrôle). En revanche, lors d’une primo-infection avec une souche non réactivable, la réactivation de la souche réinfectante était presque entièrement inhibée.La primo-infection par une souche non neurovirulente a contraint une souche, réellement virulente et inoculée secondairement, à une infection latente sans capacité de réactivation. Nous disposons ainsi des bases du développement d’une stratégie réellement préventive de l’infection herpétique récidivante, premier temps d’une éventuelle utilisation à des fins vaccinales. / The Herpes Simplex virus 1 (HSV1), whose only natural hosts are humans, can persist during the whole lifetime in a quiescent state (latent infection) in the nervous system, especially in both trigeminal ganglia (TGs, right and left), which innervate the cornea. The virus can reactivate in the TG, leading to recurrent corneal infections (keratitis) that are typically unilateral and can lead to major vision loss. To date, the only available therapies against HSV1 are curative, i.e. they control the reactivation process only after its onset. Until now, no efficient preventive treatment against HSV1 has been established, and more specifically no vaccine has been shown to be clinically effective.Our team has developed an oro-ocular murine model (based on viral inoculation in the lip), that mimics most of the aspects of the natural history of HSV1 infection in humans. In particular, lateralization is also found in this model, as only the eye ipsilateral to the inoculated lip develops keratitis (initial keratitis and recurrences), while latent virus is found in both TGs with similar levels of viral genome copies. However, the bilateral latency isn’t perfectly symmetrical at the molecular level, since the production of Latency-Associated Transcripts (LATs) and the number of LAT+ neurons are higher in the ipsilateral TG (Cavallero et al., 2014; Maillet et al., 2006). As LAT expression is associated with the capacity of the virus to reactivate, the asymmetry in LAT expression could explain the unilaterality of keratitis events.The aim of this project was to constraint a wild-type HSV1 strain to enter a non-reactivable state of latent infection in the both TGs. As this peculiar type of latent infection is observed only in the controlateral TG following a unilateral primary infection, we hypothesized that this phenomenon is linked to the kinetics of HSV1 infection in the both TGs, respectively. To test this, we studied the impact of a primary HSV1 infection on the behavior (acute phase, latency, LAT expression, capacity of reactivation) of a superinfecting HSV1 strain, inoculated at another anatomical site some days later.We have shown that the primary infection with a HSV1 strain can inhibit the pathogeny (morbidity and mortality) of a superinfecting virulent HSV1 strain, inoculated few days afterwards. Moreover, the superinfecting strain was found to be very rapidly driven in a latent state, with very poor LAT expression. This inhibitory effect also occurred when using a non-neurovirulent strain of HSV1 for the primary infection, with no further ability of the wild-type superinfecting strain to reactivate.These results clearly show that the onset of productive infection in the TGs and later on, latent infection with putative reactivation, is related to the kinetics of infection. These observations may have implications in the future for the potential development of innovative preventive strategies.

In order to eradicate HIV-1 infection the virus needs to be specifically eliminated from latently infected memory CD4+ T cells. There does not seem to be a single mechanism that promotes HIV-1 latency. RNA Polymerase II (RNAP II) pausing, chromatin structure, tissue specific transcriptional repressors and transcriptional interference have been implicated in regulating HIV-1 transcription. The transcription factor B Lymphocyte-Induced Maturation Protein 1 (Blimp-1) is expressed in B and T cells and upregulated in patients chronically infected with HIV-1. I hypothesized that Blimp-1 is a T cell intrinsic factor that binds to HIV-1 LTR, inhibits HIV-1 transcription and contributes to HIV-1 latency. Blimp-1 is expressed in primary peripheral blood CD4+ T cells and is further induced by T cell activation. Importantly, Blimp-1 is highly expressed in memory CD4+ T cells compared to naïve CD4+ T cells. Ectopic expression of Blimp-1 in CD4+ T cells represses HIV-1 transcription, whereas decreasing Blimp-1 in memory CD4+ populations activates HIV-1 transcription. Reduction of Blimp-1 in infected primary T cells increases RNAP II processivity and histone H3 acetylation. Blimp-1 binds downstream of the HIV-1 5'-LTR to the interferon-stimulated response element (ISRE) in resting primary CD4+ T cells and strongly represses Tat-dependent HIV-1 transcription. Upon T cell activation, Blimp-1 is released from the HIV-1 ISRE and this correlates with significant increase in HIV-1 transcription. These results demonstrate that Blimp-1 acts to limit HIV-1 transcription in memory CD4+ T cells and promotes the establishment and maintenance of latency. I also examined whether neighboring host promoters could impact HIV-1 transcription. Using a set of inducible cell lines I observed that neighboring promoters have minimal impact on HIV-1 transcription and that enabling release of paused RNAP II by diminishing negative elongation factor (NELF) is sufficient to reactivate transcriptionally repressed HIV-1 provirus. The implications of my results in the different mechanisms regulating HIV-1 latency are discussed.

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