Relevant bibliographies by topics / Latency

Academic literature on the topic 'Latency'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 May 2024

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Latency.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Latency"

1

Rezaei, Simin D., Hao K. Lu, J. Judy Chang, Ajantha Rhodes, Sharon R. Lewin, and Paul U. Cameron. "The Pathway To Establishing HIV Latency Is Critical to How Latency Is Maintained and Reversed." Journal of Virology 92, no. 13 (April 11, 2018): e02225-17. http://dx.doi.org/10.1128/jvi.02225-17.

Full text
Abstract:
ABSTRACTHIV infection requires lifelong antiretroviral therapy because of the persistence of latently infected CD4+T cells. The induction of virus expression from latently infected cells occurs following T cell receptor (TCR) activation, but not all latently infected cells respond to TCR stimulation. We compared two models of latently infected cells using an enhanced green fluorescent protein (EGFP) reporter virus to infect CCL19-treated resting CD4+(rCD4+) T cells (preactivation latency) or activated CD4+T cells that returned to a resting state (postactivation latency). We isolated latently infected cells by sorting for EGFP-negative (EGFP−) cells after infection. These cells were cultured with antivirals and stimulated with anti-CD3/anti-CD28, mitogens, and latency-reversing agents (LRAs) and cocultured with monocytes and anti-CD3. Spontaneous EGFP expression was more frequent in postactivation than in preactivation latency. Stimulation of latently infected cells with monocytes/anti-CD3 resulted in an increase in EGFP expression compared to that for unstimulated controls using the preactivation latency model but led to a reduction in EGFP expression in the postactivation latency model. The reduced EGFP expression was not associated with reductions in the levels of viral DNA or T cell proliferation but depended on direct contact between monocytes and T cells. Monocytes added to the postactivation latency model during the establishment of latency reduced spontaneous virus expression, suggesting that monocyte-T cell interactions at an early time point postinfection can maintain HIV latency. This direct comparison of pre- and postactivation latency suggests that effective strategies needed to reverse latency will depend on how latency is established.IMPORTANCEOne strategy being evaluated to eliminate latently infected cells that persist in HIV-infected individuals on antiretroviral therapy (ART) is to activate HIV expression or production with the goal of inducing virus-mediated cytolysis or immune-mediated clearance of infected cells. The gold standard for the activation of latent virus is T cell receptor stimulation with anti-CD3/anti-CD28. However, this stimulus activates only a small proportion of latently infected cells. We show clear differences in the responses of latently infected cells to activating stimuli based on how latent infection is established, an observation that may potentially explain the persistence of noninduced intact proviruses in HIV-infected individuals on ART.
APA, Harvard, Vancouver, ISO, and other styles
2

Virgin, Herbert W., Rachel M. Presti, Xi-Yang Li, Carl Liu, and Samuel H. Speck. "Three Distinct Regions of the Murine Gammaherpesvirus 68 Genome Are Transcriptionally Active in Latently Infected Mice." Journal of Virology 73, no. 3 (March 1, 1999): 2321–32. http://dx.doi.org/10.1128/jvi.73.3.2321-2332.1999.

Full text
Abstract:
ABSTRACT The program(s) of gene expression operating during murine gammaherpesvirus 68 (γHV68) latency is undefined, as is the relationship between γHV68 latency and latency of primate gammaherpesviruses. We used a nested reverse transcriptase PCR strategy (sensitive to approximately one copy of γHV68 genome for each genomic region tested) to screen for the presence of viral transcripts in latently infected mice. Based on the positions of known latency-associated genes in other gammaherpesviruses, we screened for the presence of transcripts corresponding to 11 open reading frames (ORFs) in the γHV68 genome in RNA from spleens and peritoneal cells of latently infected B-cell-deficient (MuMT) mice which have been shown contain high levels of reactivable latent γHV68 (K. E. Weck, M. L. Barkon, L. I. Yoo, S. H. Speck, and H. W. Virgin, J. Virol. 70:6775–6780, 1996). To control for the possible presence of viral lytic activity, we determined that RNA from latently infected peritoneal and spleen cells contained few or no detectable transcripts corresponding to seven ORFs known to encode viral gene products associated with lytic replication. However, we did detect low-level expression of transcripts arising from the region of gene 50 (encoding the putative homolog of the Epstein-Barr virus BRLF1 transactivator) in peritoneal but not spleen cells. Latently infected peritoneal cells consistently scored for expression of RNA derived from 4 of the 11 candidate latency-associated ORFs examined, including the regions of ORF M2, ORF M11 (encoding v-bcl-2), gene 73 (a homolog of the Kaposi’s sarcoma-associated herpesvirus [human herpesvirus 8] gene encoding latency-associated nuclear antigen), and gene 74 (encoding a G-protein coupled receptor homolog, v-GCR). Latently infected spleen cells consistently scored positive for RNA derived from 3 of the 11 candidate latency-associated ORFs examined, including ORF M2, ORF M3, and ORF M9. To further characterize transcription of these candidate latency-associated ORFs, we examined their transcription in lytically infected fibroblasts by Northern analysis. We detected abundant transcription from regions of the genome containing ORF M3 and ORF M9, as well as the known lytic-cycle genes. However, transcription of ORF M2, ORF M11, gene 73, and gene 74 was barely detectable in lytically infected fibroblasts, consistent with a role of these viral genes during latent infection. We conclude that (i) we have identified several candidate latency genes of murine γHV68, (ii) expression of genes during latency may be different in different organs, consistent with multiple latency programs and/or multiple cellular sites of latency, and (iii) regions of the viral genome (v-bcl-2 gene, v-GCR gene, and gene 73) are transcribed during latency with both γHV68 and primate gammaherpesviruses. The implications of these findings for replacing previous operational definitions of γHV68 latency with a molecular definition are discussed.
APA, Harvard, Vancouver, ISO, and other styles
3

Jefferys, Stuart R., Samuel D. Burgos, Jackson J. Peterson, Sara R. Selitsky, Anne-Marie W. Turner, Lindsey I. James, Yi-Hsuan Tsai, et al. "Epigenomic characterization of latent HIV infection identifies latency regulating transcription factors." PLOS Pathogens 17, no. 2 (February 26, 2021): e1009346. http://dx.doi.org/10.1371/journal.ppat.1009346.

Full text
Abstract:
Transcriptional silencing of HIV in CD4 T cells generates a reservoir of latently infected cells that can reseed infection after interruption of therapy. As such, these cells represent the principal barrier to curing HIV infection, but little is known about their characteristics. To further our understanding of the molecular mechanisms of latency, we characterized a primary cell model of HIV latency in which infected cells adopt heterogeneous transcriptional fates. In this model, we observed that latency is a stable, heritable state that is transmitted through cell division. Using Assay of Transposon-Accessible Chromatin sequencing (ATACseq) we found that latently infected cells exhibit greatly reduced proviral accessibility, indicating the presence of chromatin-based structural barriers to viral gene expression. By quantifying the activity of host cell transcription factors, we observe elevated activity of Forkhead and Kruppel-like factor transcription factors (TFs), and reduced activity of AP-1, RUNX and GATA TFs in latently infected cells. Interestingly, latency reversing agents with different mechanisms of action caused distinct patterns of chromatin reopening across the provirus. We observe that binding sites for the chromatin insulator CTCF are highly enriched in the differentially open chromatin of infected CD4 T cells. Furthermore, depletion of CTCF inhibited HIV latency, identifying this factor as playing a key role in the initiation or enforcement of latency. These data indicate that HIV latency develops preferentially in cells with a distinct pattern of TF activity that promotes a closed proviral structure and inhibits viral gene expression. Furthermore, these findings identify CTCF as a novel regulator of HIV latency.
APA, Harvard, Vancouver, ISO, and other styles
4

Maillet, Séverine, Thierry Naas, Sophie Crepin, Anne-Marie Roque-Afonso, Florence Lafay, Stacey Efstathiou, and Marc Labetoulle. "Herpes Simplex Virus Type 1 Latently Infected Neurons Differentially Express Latency-Associated and ICP0 Transcripts." Journal of Virology 80, no. 18 (September 15, 2006): 9310–21. http://dx.doi.org/10.1128/jvi.02615-05.

Full text
Abstract:
ABSTRACT During the latent phase of herpes simplex virus type 1 (HSV-1) infection, the latency-associated transcripts (LATs) are the most abundant viral transcripts present in neurons, but some immediate-early viral transcripts, such as those encoding ICP0, have also been reported to be transcribed in latently infected mouse trigeminal ganglia (TG). A murine oro-ocular model of herpetic infection was used to study ICP0 gene expression in the major anatomical sites of HSV-1 latency, including the TG, superior cervical ganglion, spinal cord, and hypothalamus. An HSV-1 recombinant strain, SC16 110LacZ, revealed ICP0 promoter activity in several neurons in latently infected ganglia, and following infection with wild-type HSV-1 strain SC16, in situ hybridization analyses identified ICP0 transcripts in the nuclei of neurons at times consistent with the establishment of latency. Reverse transcription (RT)-PCR assays performed on RNA extracted from latently infected tissues indicated that ICP0 transcripts were detected in all anatomical sites of viral latency. Furthermore, quantitative real-time RT-PCR showed that neurons differentially expressed the LATs and ICP0 transcripts, with splicing of ICP0 transcripts being dependent on the anatomical location of latency. Finally, TG neurons were characterized by high-level expression of LATs and detection of abundant unspliced ICP0 transcripts, a pattern markedly different from those of other anatomical sites of HSV-1 latency. These results suggest that LATs might be involved in the maintenance of HSV-1 latency through the posttranscriptional regulation of ICP0 in order to inhibit expression of this potent activator of gene expression during latency.
APA, Harvard, Vancouver, ISO, and other styles
5

Usherwood, Edward J., Douglas J. Roy, Kim Ward, Sherri L. Surman, Bernadette M. Dutia, Marcia A. Blackman, James P. Stewart, and David L. Woodland. "Control of Gammaherpesvirus Latency by Latent Antigen-Specific Cd8+ T Cells." Journal of Experimental Medicine 192, no. 7 (September 25, 2000): 943–52. http://dx.doi.org/10.1084/jem.192.7.943.

Full text
Abstract:
The contribution of the latent antigen-specific CD8+ T cell response to the control of gammaherpesvirus latency is currently obscure. Some latent antigens induce potent T cell responses, but little is known about their induction or the role they play during the establishment of latency. Here we used the murine gammaherpesvirus system to examine the expression of the latency-associated M2 gene during latency and the induction of the CD8+ T cell response to this protein. M2, in contrast to the M3 latency-associated antigen, was expressed at day 14 after infection but was undetectable during long-term latency. The induction of the M291–99/Kd CD8+ T cell response was B cell dependent, transient, and apparently induced by the rapid increase in latently infected cells around day 14 after intranasal infection. These kinetics were consistent with a role in controlling the initial “burst” of latently infected cells. In support of this hypothesis, adoptive transfer of an M2-specific CD8+ T cell line reduced the initial load of latently infected cells, although not the long-term load. These data represent the first description of a latent antigen-specific immune response in this model, and suggest that vaccination with latent antigens such as M2 may be capable of modulating latent gammaherpesvirus infection.
APA, Harvard, Vancouver, ISO, and other styles
6

Liu, Yilin, Morgan Hancock, Aspen Workman, Alan Doster, and Clinton Jones. "β-Catenin, a Transcription Factor Activated by Canonical Wnt Signaling, Is Expressed in Sensory Neurons of Calves Latently Infected with Bovine Herpesvirus 1." Journal of Virology 90, no. 6 (January 6, 2016): 3148–59. http://dx.doi.org/10.1128/jvi.02971-15.

Full text
Abstract:
ABSTRACTLike manyAlphaherpesvirinaesubfamily members, bovine herpesvirus 1 (BoHV-1) expresses an abundant transcript in latently infected sensory neurons, the latency-related (LR)-RNA. LR-RNA encodes a protein (ORF2) that inhibits apoptosis, interacts with Notch family members, interferes with Notch-mediated transcription, and stimulates neurite formation in cells expressing Notch. An LR mutant virus containing stop codons at the amino terminus of ORF2 does not reactivate from latency or replicate efficiently in certain tissues, indicating that LR gene products are important. In this study, β-catenin, a transcription factor activated by the canonical Wnt signaling pathway, was frequently detected in ORF2-positive trigeminal ganglionic neurons of latently infected, but not mock-infected, calves. Conversely, the lytic cycle regulatory protein (BoHV-1 infected cell protein 0, or bICP0) was not frequently detected in β-catenin-positive neurons in latently infected calves. During dexamethasone-induced reactivation from latency, mRNA expression levels of two Wnt antagonists, Dickkopf-1 (DKK-1) and secreted Frizzled-related protein 2 (SFRP2), were induced in bovine trigeminal ganglia (TG), which correlated with reduced β-catenin protein expression in TG neurons 6 h after dexamethasone treatment. ORF2 and a coactivator of β-catenin, mastermind-like protein 1 (MAML1), stabilized β-catenin protein levels and stimulated β-catenin-dependent transcription in mouse neuroblastoma cells more effectively than MAML1 or ORF2 alone. Neuroblastoma cells expressing ORF2, MAML1, and β-catenin were highly resistant to cell death following serum withdrawal, whereas most cells transfected with only one of these genes died. The Wnt signaling pathway interferes with neurodegeneration but promotes neuronal differentiation, suggesting that stabilization of β-catenin expression by ORF2 promotes neuronal survival and differentiation.IMPORTANCEBovine herpesvirus 1 (BoHV-1) is an important pathogen of cattle, and like manyAlphaherpesvirinaesubfamily members establishes latency in sensory neurons. Lifelong latency and the ability to reactivate from latency are crucial for virus transmission. Maintaining the survival and normal functions of terminally differentiated neurons is also crucial for lifelong latency. Our studies revealed that BoHV-1 gene products expressed during latency stabilize expression of the transcription factor β-catenin and perhaps its cofactor, mastermind-like protein 1 (MAML1). In contrast to expression during latency, β-catenin expression in sensory neurons is not detectable following treatment of latently infected calves with the synthetic corticosteroid dexamethasone to initiate reactivation from latency. A viral protein (ORF2) expressed in a subset of latently infected neurons stabilized β-catenin and MAML1 in transfected cells. ORF2, β-catenin, and MAML1 also enhanced cell survival when growth factors were withdrawn, suggesting that these genes enhance survival of latently infected neurons.
APA, Harvard, Vancouver, ISO, and other styles
7

Taura, Manabu, Eric Song, Ya-Chi Ho, and Akiko Iwasaki. "Apobec3A maintains HIV-1 latency through recruitment of epigenetic silencing machinery to the long terminal repeat." Proceedings of the National Academy of Sciences 116, no. 6 (January 22, 2019): 2282–89. http://dx.doi.org/10.1073/pnas.1819386116.

Full text
Abstract:
HIV-1 integrates into the genome of target cells and establishes latency indefinitely. Understanding the molecular mechanism of HIV-1 latency maintenance is needed for therapeutic strategies to combat existing infection. In this study, we found an unexpected role for Apobec3A (apolipoprotein B MRNA editing enzyme catalytic subunit 3A, abbreviated “A3A”) in maintaining the latency state within HIV-1–infected cells. Overexpression of A3A in latently infected cell lines led to lower reactivation, while knockdown or knockout of A3A led to increased spontaneous and inducible HIV-1 reactivation. A3A maintains HIV-1 latency by associating with proviral DNA at the 5′ long terminal repeat region, recruiting KAP1 and HP1, and imposing repressive histone marks. We show that knockdown of A3A in latently infected human primary CD4 T cells enhanced HIV-1 reactivation. Collectively, we provide evidence and a mechanism by which A3A reinforces HIV-1 latency in infected CD4 T cells.
APA, Harvard, Vancouver, ISO, and other styles
8

Satheesan, Sangeetha, Haitang Li, John C. Burnett, Mayumi Takahashi, Shasha Li, Shiny Xiaqin Wu, Timothy W. Synold, John J. Rossi, and Jiehua Zhou. "HIV Replication and Latency in a Humanized NSG Mouse Model during Suppressive Oral Combinational Antiretroviral Therapy." Journal of Virology 92, no. 7 (January 17, 2018): e02118-17. http://dx.doi.org/10.1128/jvi.02118-17.

Full text
Abstract:
ABSTRACTAlthough current combinatorial antiretroviral therapy (cART) is therapeutically effective in the majority of HIV patients, interruption of therapy can cause a rapid rebound in viremia, demonstrating the existence of a stable reservoir of latently infected cells. HIV latency is therefore considered a primary barrier to HIV eradication. Identifying, quantifying, and purging the HIV reservoir is crucial to effectively curing patients and relieving them from the lifelong requirement for therapy. Latently infected transformed cell models have been used to investigate HIV latency; however, these models cannot accurately represent the quiescent cellular environment of primary latently infected cellsin vivo. For this reason,in vivohumanized murine models have been developed for screening antiviral agents, identifying latently infected T cells, and establishing treatment approaches for HIV research. Such models include humanized bone marrow/liver/thymus mice and SCID-hu-thy/liv mice, which are repopulated with human immune cells and implanted human tissues through laborious surgical manipulation. However, no one has utilized the human hematopoietic stem cell-engrafted NOD/SCID/IL2rγnull(NSG) model (hu-NSG) for this purpose. Therefore, in the present study, we used the HIV-infected hu-NSG mouse to recapitulate the key aspects of HIV infection and pathogenesisin vivo. Moreover, we evaluated the ability of HIV-infected human cells isolated from HIV-infected hu-NSG mice on suppressive cART to act as a latent HIV reservoir. Our results demonstrate that the hu-NSG model is an effective surgery-freein vivosystem in which to efficiently evaluate HIV replication, antiretroviral therapy, latency and persistence, and eradication interventions.IMPORTANCEHIV can establish a stably integrated, nonproductive state of infection at the level of individual cells, known as HIV latency, which is considered a primary barrier to curing HIV. A complete understanding of the establishment and role of HIV latencyin vivowould greatly enhance attempts to develop novel HIV purging strategies. An ideal animal model for this purpose should be easy to work with, should have a shortened disease course so that efficacy testing can be completed in a reasonable time, and should have immune correlates that are easily translatable to humans. We therefore describe a novel application of the hematopoietic stem cell-transplanted humanized NSG model for dynamically testing antiretroviral treatment, supporting HIV infection, establishing HIV latencyin vivo. The hu-NSG model could be a facile alternative to humanized bone marrow/liver/thymus or SCID-hu-thy/liv mice in which laborious surgical manipulation and time-consuming human cell reconstitution is required.
APA, Harvard, Vancouver, ISO, and other styles
9

Jones, Clinton. "Herpes Simplex Virus Type 1 and Bovine Herpesvirus 1 Latency." Clinical Microbiology Reviews 16, no. 1 (January 2003): 79–95. http://dx.doi.org/10.1128/cmr.16.1.79-95.2003.

Full text
Abstract:
SUMMARY Primary infection by herpes simplex virus type 1 (HSV-1) can cause clinical symptoms in the peripheral and central nervous system, upper respiratory tract, and gastrointestinal tract. Recurrent ocular shedding leads to corneal scarring that can progress to vision loss. Consequently, HSV-1 is the leading cause of corneal blindness due to an infectious agent. Bovine herpesvirus 1 (BHV-1) has similar biological properties to HSV-1 and is a significant health concern to the cattle industry. Latency of BHV-1 and HSV-1 is established in sensory neurons of trigeminal ganglia, but latency can be interrupted periodically, leading to reactivation from latency and spread of infectious virus. The ability of HSV-1 and BHV-1 to reactivate from latency leads to virus transmission and can lead to recurrent disease in individuals latently infected with HSV-1. During latency, the only abundant HSV-1 RNA expressed is the latency-associated transcript (LAT). In latently infected cattle, the latency-related (LR) RNA is the only abundant transcript that is expressed. LAT and LR RNA are antisense to ICP0 or bICP0, viral genes that are crucial for productive infection, suggesting that LAT and LR RNA interfere with productive infection by inhibiting ICP0 or bICP0 expression. Numerous studies have concluded that LAT expression is important for the latency-reactivation cycle in animal models. The LR gene has recently been demonstrated to be required for the latency-reactivation cycle in cattle. Several recent studies have demonstrated that LAT and the LR gene inhibit apoptosis (programmed cell death) in trigeminal ganglia of infected animals and transiently transfected cells. The antiapoptotic properties of LAT map to the same sequences that are necessary for promoting reactivation from latency. This review summarizes our current knowledge of factors regulating the latency-reactivation cycle of HSV-1 and BHV-1.
APA, Harvard, Vancouver, ISO, and other styles
10

Tibbetts, Scott A., Linda F. van Dyk, Samuel H. Speck, and Herbert W. Virgin. "Immune Control of the Number and Reactivation Phenotype of Cells Latently Infected with a Gammaherpesvirus." Journal of Virology 76, no. 14 (July 15, 2002): 7125–32. http://dx.doi.org/10.1128/jvi.76.14.7125-7132.2002.

Full text
Abstract:
ABSTRACT Despite active immune responses, gammaherpesviruses establish latency. In a related process, these viruses also persistently replicate by using a mechanism that requires different viral genes than acute-phase replication. Many questions remain about the role of immunity in chronic gammaherpesvirus infection, including whether the immune system controls latency by regulating latent cell numbers and/or other properties and what specific immune mediators control latency and persistent replication. We show here that CD8+ T cells regulate both latency and persistent replication and demonstrate for the first time that CD8+ T cells regulate both the number of latently infected cells and the efficiency with which infected cells reactivate from latency. Furthermore, we show that gamma interferon (IFN-γ) and perforin, which play no significant role during acute infection, are essential for immune control of latency and persistent replication. Surprisingly, the effects of perforin and IFN-γ are site specific, with IFN-γ being important in peritoneal cells while perforin is important in the spleen. Studies of the mechanisms of action of IFN-γ and perforin revealed that perforin acts primarily by controlling the number of latently infected cells while IFN-γ acts primarily by controlling reactivation efficiency. The immune system therefore controls chronic gammaherpesvirus infection by site-specific mechanisms that regulate both the number and reactivation phenotype of latently infected cells.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Latency"

1

Marxer, Piñón Ricard. "Audio source separation for music in low-latency and high-latency scenarios." Doctoral thesis, Universitat Pompeu Fabra, 2013. http://hdl.handle.net/10803/123808.

Full text
Abstract:
Aquesta tesi proposa mètodes per tractar les limitacions de les tècniques existents de separació de fonts musicals en condicions de baixa i alta latència. En primer lloc, ens centrem en els mètodes amb un baix cost computacional i baixa latència. Proposem l'ús de la regularització de Tikhonov com a mètode de descomposició de l'espectre en el context de baixa latència. El comparem amb les tècniques existents en tasques d'estimació i seguiment dels tons, que són passos crucials en molts mètodes de separació. A continuació utilitzem i avaluem el mètode de descomposició de l'espectre en tasques de separació de veu cantada, baix i percussió. En segon lloc, proposem diversos mètodes d'alta latència que milloren la separació de la veu cantada, gràcies al modelatge de components específics, com la respiració i les consonants. Finalment, explorem l'ús de correlacions temporals i anotacions manuals per millorar la separació dels instruments de percussió i dels senyals musicals polifònics complexes.
Esta tesis propone métodos para tratar las limitaciones de las técnicas existentes de separación de fuentes musicales en condiciones de baja y alta latencia. En primer lugar, nos centramos en los métodos con un bajo coste computacional y baja latencia. Proponemos el uso de la regularización de Tikhonov como método de descomposición del espectro en el contexto de baja latencia. Lo comparamos con las técnicas existentes en tareas de estimación y seguimiento de los tonos, que son pasos cruciales en muchos métodos de separación. A continuación utilizamos y evaluamos el método de descomposición del espectro en tareas de separación de voz cantada, bajo y percusión. En segundo lugar, proponemos varios métodos de alta latencia que mejoran la separación de la voz cantada, gracias al modelado de componentes que a menudo no se toman en cuenta, como la respiración y las consonantes. Finalmente, exploramos el uso de correlaciones temporales y anotaciones manuales para mejorar la separación de los instrumentos de percusión y señales musicales polifónicas complejas.
This thesis proposes specific methods to address the limitations of current music source separation methods in low-latency and high-latency scenarios. First, we focus on methods with low computational cost and low latency. We propose the use of Tikhonov regularization as a method for spectrum decomposition in the low-latency context. We compare it to existing techniques in pitch estimation and tracking tasks, crucial steps in many separation methods. We then use the proposed spectrum decomposition method in low-latency separation tasks targeting singing voice, bass and drums. Second, we propose several high-latency methods that improve the separation of singing voice by modeling components that are often not accounted for, such as breathiness and consonants. Finally, we explore using temporal correlations and human annotations to enhance the separation of drums and complex polyphonic music signals.
APA, Harvard, Vancouver, ISO, and other styles
2

Wang, Yonghao. "Low latency audio processing." Thesis, Queen Mary, University of London, 2018. http://qmro.qmul.ac.uk/xmlui/handle/123456789/44697.

Full text
Abstract:
Latency in the live audio processing chain has become a concern for audio engineers and system designers because significant delays can be perceived and may affect synchronisation of signals, limit interactivity, degrade sound quality and cause acoustic feedback. In recent years, latency problems have become more severe since audio processing has become digitised, high-resolution ADCs and DACs are used, complex processing is performed, and data communication networks are used for audio signal transmission in conjunction with other traffic types. In many live audio applications, latency thresholds are bounded by human perceptions. The applications such as music ensembles and live monitoring require low delay and predictable latency. Current digital audio systems either have difficulties to achieve or have to trade-off latency with other important audio processing functionalities. This thesis investigated the fundamental causes of the latency in a modern digital audio processing system: group delay, buffering delay, and physical propagation delay and their associated system components. By studying the time-critical path of a general audio system, we focus on three main functional blocks that have the significant impact on overall latency; the high-resolution digital filters in sigma-delta based ADC/DAC, the operating system to process low latency audio streams, and the audio networking to transmit audio with flexibility and convergence. In this work, we formed new theory and methods to reduce latency and accurately predict latency for group delay. We proposed new scheduling algorithms for the operating system that is suitable for low latency audio processing. We designed a new system architecture and new protocols to produce deterministic networking components that can contribute the overall timing assurance and predictability of live audio processing. The results are validated by simulations and experimental tests. Also, this bottom-up approach is aligned with the methodology that could solve the timing problem of general cyber-physical systems that require the integration of communication, software and human interactions.
APA, Harvard, Vancouver, ISO, and other styles
3

Riddoch, David James. "Low latency distributed computing." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619850.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Hardwick, David R., and na. "Factors Associated with Saccade Latency." Griffith University. School of Psychology, 2008. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20100705.111516.

Full text
Abstract:
Part of the aim of this thesis was to explore a model for producing very fast saccade latencies in the 80 to 120ms range. Its primary motivation was to explore a possible interaction by uniquely combining three independent saccade factors: the gap effect, target-feature-discrimination, and saccadic inhibition of return (IOR). Its secondary motivation was to replicate (in a more conservative and tightly controlled design) the surprising findings of Trottier and Pratt (2005), who found that requiring a high resolution task at the saccade target location speeded saccades, apparently by disinhibition. Trottier and Pratt’s finding was so surprising it raised the question: Could the oculomotor braking effect of saccadic IOR to previously viewed locations be reduced or removed by requiring a high resolution task at the target location? Twenty naïve untrained undergraduate students participated in exchange for course credit. Multiple randomised temporal and spatial target parameters were introduced in order to increase probability of exogenous responses. The primary measured variable was saccade latency in milliseconds, with the expectation of higher probability of very fast saccades (i.e. 80-120ms). Previous research suggested that these very fast saccades could be elicited in special testing circumstances with naïve participants, such as during the gap task, or in highly trained observers in non-gap tasks (Fischer & Weber, 1993). Trottier and Pratt (2005) found that adding a task demand that required naïve untrained participants to obtain a feature of the target stimulus (and to then make a discriminatory decision) also produced a higher probability of very fast saccade latencies. They stated that these saccades were not the same as saccade latencies previously referred to as express saccades produced in the gap paradigm, and proposed that such very fast saccades were normal. Carpenter (2001) found that in trained participants the probability of finding very fast saccades during the gap task increased when the horizontal direction of the current saccade continued in the same direction as the previous saccade (as opposed to reversing direction) – giving a distinct bimodality in the distribution of latencies in five out of seven participants, and likened his findings to the well known IOR effect. The IOR effect has previously been found in both manual key-press RT and saccadic latency paradigms. Hunt and Kingstone (2003) stated that there were both cortical top-down and oculomotor hard-wired aspects to IOR. An experiment was designed that included obtain-target-feature and oculomotor-prior-direction, crossed with two gap level offsets (0ms & 200ms-gap). Target-feature discrimination accuracy was high (97%). Under-additive main effects were found for each factor, with a three-way interaction effect for gap by obtain-feature by oculomotor-prior-direction. Another new three-way interaction was also found for anticipatory saccade type. Anticipatory saccades became significantly more likely under obtain-target-feature for the continuing oculomotor direction. This appears to be a similar effect to the increased anticipatory direction-error rate in the antisaccade task. These findings add to the saccadic latency knowledge base and in agreement with both Carpenter and Trottier and Pratt, laboratory testing paradigms can affect saccadic latency distributions. That is, salient (meaningful) targets that follow more natural oculomotor trajectories produce higher probability of very fast latencies in the 80-120ms range. In agreement with Hunt and Kingstone, there appears to be an oculomotor component to IOR. Specifically, saccadic target-prior-location interacts differently for obtain-target-feature under 200-ms gap than under 0ms-gap, and is most likely due predominantly to a predictive disinhibitory oculomotor momentum effect, rather than being due to the attentional inhibitory effect proposed for key-press IOR. A new interpretation for the paradigm previously referred to as IOR is offered that includes a link to the smooth pursuit system. Additional studies are planned to explore saccadic interactions in more detail.
APA, Harvard, Vancouver, ISO, and other styles
5

Zieliń́ski, Piotr. "Minimizing latency of agreement protocols." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.613987.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Tran, Tony V. H. "IPv6 geolocation using latency constraints." Thesis, Monterey, California: Naval Postgraduate School, 2014. http://hdl.handle.net/10945/41452.

Full text
Abstract:
Approved for public release; distribution is unlimited.
IPv4 addresses are now exhausted, and as a result, the growth of IPv6 addresses has increased significantly since 2010. The rate of increase of IPv6 usage is expected to continue; thus the need to determine the geographic location of IPv6 hosts will grow to support location-aware applications. Examples of services that require or benefit from IPv6 geolocation include overlay networks, location-based security mechanisms, client language and policy determination, and location targeted advertising. Internet protocol (IP) geolocation is the process of obtaining the geographical location of a device or host using only the host’s IP address. This study looked at using constraint-based geolocation (CBG), a latency-based measurement technique, on IPv6 infrastructure and analyzed location accuracy against ground truth. Results show that overall IPv6 CBG had up to 30% larger average error distance estimates as compared to IPv4 CBG. However, CBG performance varied depending on the location of the target host. Hosts located in the Asia-Pacific region performed the worst, while hosts located in Europe had the best performance in median error distance. AS-level path differences between IPv4 and IPv6 and the number of landmarks had the most significant impact on CBG performance.
APA, Harvard, Vancouver, ISO, and other styles
7

Lua, Eng Keong. "The structure of Internet latency." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.613027.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Yoo, Sirah. "Ineffable: Latency in Symbolic Languages." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4814.

Full text
Abstract:
The design process demands comprehensive knowledge of visual signs and symbols with a focus on visual literacy; it is related to visual syntax, semantics, and the pragmatics of contexts. My work is an interdisciplinary investigation into how designers integrate polysemantic signs into their design process for particular and highly individualized audiences. By analyzing the role of signs in specific contexts across the spectrum of arts, society, literature, and semiotics, a designer's understanding of the cyclical nature of interpretation and reinterpretation in complex environments creates an avenue for cultivating a new schema that provides further levels of interpretations and different access points. By removing elements from their original context, and fusing these elements into new narratives, we implement new meanings and emphasize the value of interpretation.
APA, Harvard, Vancouver, ISO, and other styles
9

Hardwick, David R. "Factors Associated with Saccade Latency." Thesis, Griffith University, 2008. http://hdl.handle.net/10072/365963.

Full text
Abstract:
Part of the aim of this thesis was to explore a model for producing very fast saccade latencies in the 80 to 120ms range. Its primary motivation was to explore a possible interaction by uniquely combining three independent saccade factors: the gap effect, target-feature-discrimination, and saccadic inhibition of return (IOR). Its secondary motivation was to replicate (in a more conservative and tightly controlled design) the surprising findings of Trottier and Pratt (2005), who found that requiring a high resolution task at the saccade target location speeded saccades, apparently by disinhibition. Trottier and Pratt’s finding was so surprising it raised the question: Could the oculomotor braking effect of saccadic IOR to previously viewed locations be reduced or removed by requiring a high resolution task at the target location? Twenty naïve untrained undergraduate students participated in exchange for course credit. Multiple randomised temporal and spatial target parameters were introduced in order to increase probability of exogenous responses. The primary measured variable was saccade latency in milliseconds, with the expectation of higher probability of very fast saccades (i.e. 80-120ms). Previous research suggested that these very fast saccades could be elicited in special testing circumstances with naïve participants, such as during the gap task, or in highly trained observers in non-gap tasks (Fischer & Weber, 1993). Trottier and Pratt (2005) found that adding a task demand that required naïve untrained participants to obtain a feature of the target stimulus (and to then make a discriminatory decision) also produced a higher probability of very fast saccade latencies. They stated that these saccades were not the same as saccade latencies previously referred to as express saccades produced in the gap paradigm, and proposed that such very fast saccades were normal. Carpenter (2001) found that in trained participants the probability of finding very fast saccades during the gap task increased when the horizontal direction of the current saccade continued in the same direction as the previous saccade (as opposed to reversing direction) – giving a distinct bimodality in the distribution of latencies in five out of seven participants, and likened his findings to the well known IOR effect. The IOR effect has previously been found in both manual key-press RT and saccadic latency paradigms. Hunt and Kingstone (2003) stated that there were both cortical top-down and oculomotor hard-wired aspects to IOR. An experiment was designed that included obtain-target-feature and oculomotor-prior-direction, crossed with two gap level offsets (0ms & 200ms-gap). Target-feature discrimination accuracy was high (97%). Under-additive main effects were found for each factor, with a three-way interaction effect for gap by obtain-feature by oculomotor-prior-direction. Another new three-way interaction was also found for anticipatory saccade type. Anticipatory saccades became significantly more likely under obtain-target-feature for the continuing oculomotor direction. This appears to be a similar effect to the increased anticipatory direction-error rate in the antisaccade task. These findings add to the saccadic latency knowledge base and in agreement with both Carpenter and Trottier and Pratt, laboratory testing paradigms can affect saccadic latency distributions. That is, salient (meaningful) targets that follow more natural oculomotor trajectories produce higher probability of very fast latencies in the 80-120ms range. In agreement with Hunt and Kingstone, there appears to be an oculomotor component to IOR. Specifically, saccadic target-prior-location interacts differently for obtain-target-feature under 200-ms gap than under 0ms-gap, and is most likely due predominantly to a predictive disinhibitory oculomotor momentum effect, rather than being due to the attentional inhibitory effect proposed for key-press IOR. A new interpretation for the paradigm previously referred to as IOR is offered that includes a link to the smooth pursuit system. Additional studies are planned to explore saccadic interactions in more detail.
Thesis (Masters)
Master of Philosophy (MPhil)
School of Psychology
Griffith Health
Full Text
APA, Harvard, Vancouver, ISO, and other styles
10

Poccardi, Nolwenn. "Etude du contrôle de l’etablissement de l’infection latente de HSV1 et de sa capacité de réactivation." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS148.

Full text
Abstract:
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
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Latency"

1

1957-, Pomerantz Roger J., ed. Retroviral latency. Austin: R.G. Landes, 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Silvestri, Guido, and Mathias Lichterfeld, eds. HIV-1 Latency. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-02816-9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Minarovits, Janos, Eva Gonczol, and Tibor Valyi-Nagy, eds. Latency Strategies of Herpesviruses. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-34127-9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Latency paradox of Barret Trufflehard. [Place of publication not identified]: [publisher not identified], 2015.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Psychotherapeutic strategies in the latency years. Northvale, N.J: Aronson, 1987.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Epstein-Barr virus: Latency and transformation. Wymondham, Norfolk, UK: Caister Academic Press, 2010.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Agnes, Matthias, Bautzner69 Ausstellungsraum (Dresden Germany), and Bautzener Kunstverein, eds. Evelyn Richter: Von der Latenz der Bilder = on the latency of images. Dresden: Hesperus Print Verlag, 2018.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Credle, Rufus. WebSphere MQ low latency messaging development guide. [United States]: IBM International Technical Support Organization, 2009.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Center, Langley Research, ed. Low latency messages on distributed memory multiprocessors. Hampton, Va: National Aeronautics and Space Administration, Langley Research Center, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Center, Langley Research, ed. Low latency messages on distributed memory multiprocessors. Hampton, Va: National Aeronautics and Space Administration, Langley Research Center, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Latency"

1

Mehlhorn, Heinz. "Latency." In Encyclopedia of Parasitology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_1713-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Mehlhorn, Heinz. "Latency." In Encyclopedia of Parasitology, 1424. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_1713.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Lewis, Moira, Courtenay Norbury, Rhiannon Luyster, Lauren Schmitt, Andrea McDuffie, Eileen Haebig, Donna S. Murray, et al. "Latency." In Encyclopedia of Autism Spectrum Disorders, 1698. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1698-3_100792.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Weik, Martin H. "latency." In Computer Science and Communications Dictionary, 877. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/1-4020-0613-6_9995.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Gooch, Jan W. "Latency." In Encyclopedic Dictionary of Polymers, 903. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14092.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Li, Guoliang, Jiannan Wang, Yudian Zheng, Ju Fan, and Michael J. Franklin. "Latency Control." In Crowdsourced Data Management, 63–70. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-7847-7_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Ritvo, Ariella Riva, Fred R. Volkmar, Karen M. Lionello-Denolf, Trina D. Spencer, James Todd, Nurit Yirmiya, Maya Yaari, et al. "Response Latency." In Encyclopedia of Autism Spectrum Disorders, 2574–75. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1698-3_1045.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Weik, Martin H. "ring latency." In Computer Science and Communications Dictionary, 1497. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/1-4020-0613-6_16420.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Dongarra, Jack, Piotr Luszczek, Paul Feautrier, Field G. Zee, Ernie Chan, Robert A. Geijn, Robert Bjornson, et al. "Latency Hiding." In Encyclopedia of Parallel Computing, 1006. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-0-387-09766-4_415.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Bendiske, Stephanie. "Response Latency." In Encyclopedia of Autism Spectrum Disorders, 3949. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-91280-6_1045.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Latency"

1

Fischer, Martin J., Denise M. Bevilacqua Masi, and John F. Shortle. "Approximating Low Latency Queueing Buffer Latency." In 2008 Fourth Advanced International Conference on Telecommunications (AICT). IEEE, 2008. http://dx.doi.org/10.1109/aict.2008.7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Yu, Minlan, Marina Thottan, and Li Li. "Latency equalization." In the ACM workshop. New York, New York, USA: ACM Press, 2008. http://dx.doi.org/10.1145/1397718.1397728.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Stauffert, Jan-Philipp, Florian Niebling, and Marc Erich Latoschik. "A Latency and Latency Jitter Simulation Framework with OSVR." In 2017 IEEE 10th Workshop on Software Engineering and Architectures for Realtime Interactive Systems (SEARIS). IEEE, 2017. http://dx.doi.org/10.1109/searis41720.2017.9183433.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Claypool, Mark, and Kajal Claypool. "Latency can kill." In the first annual ACM SIGMM conference. New York, New York, USA: ACM Press, 2010. http://dx.doi.org/10.1145/1730836.1730863.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Olano, Marc, Jon Cohen, Mark Mine, and Gary Bishop. "Combatting rendering latency." In the 1995 symposium. New York, New York, USA: ACM Press, 1995. http://dx.doi.org/10.1145/199404.199407.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Xia, Haijun, Ricardo Jota, Benjamin McCanny, Zhe Yu, Clifton Forlines, Karan Singh, and Daniel Wigdor. "Zero-latency tapping." In UIST '14: The 27th Annual ACM Symposium on User Interface Software and Technology. New York, NY, USA: ACM, 2014. http://dx.doi.org/10.1145/2642918.2647348.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Maric, I. "Low latency communications." In 2013 Information Theory and Applications Workshop (ITA 2013). IEEE, 2013. http://dx.doi.org/10.1109/ita.2013.6502956.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Feria, Erlan H. "Latency-information theory." In 2010 IEEE Sarnoff Symposium. IEEE, 2010. http://dx.doi.org/10.1109/sarnof.2010.5469775.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Mansley, Kieran, David Scott, Alastair Tse, and Anil Madhavapeddy. "Feedback, latency, accuracy." In ACM SIGCOMM 2004 workshops. New York, New York, USA: ACM Press, 2004. http://dx.doi.org/10.1145/1016540.1016544.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Flach, Tobias, Nandita Dukkipati, Andreas Terzis, Barath Raghavan, Neal Cardwell, Yuchung Cheng, Ankur Jain, Shuai Hao, Ethan Katz-Bassett, and Ramesh Govindan. "Reducing web latency." In SIGCOMM'13: ACM SIGCOMM 2013 Conference. New York, NY, USA: ACM, 2013. http://dx.doi.org/10.1145/2486001.2486014.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Latency"

1

Finn, N., J. Y. Le Boudec, E. Mohammadpour, J. Zhang, and B. Varga. Deterministic Networking (DetNet) Bounded Latency. RFC Editor, November 2022. http://dx.doi.org/10.17487/rfc9320.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

El, K., ed. Low-Latency Handoffs in Mobile IPv4. RFC Editor, June 2007. http://dx.doi.org/10.17487/rfc4881.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Stricker, Lawrence J., and David L. Alterton. Response Latency Measures for Biographical Inventories. Fort Belvoir, VA: Defense Technical Information Center, March 1991. http://dx.doi.org/10.21236/ada234988.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Stricker, Lawrence J., and David L. Alderton. Response Latency Measures for Biographical Inventories. Fort Belvoir, VA: Defense Technical Information Center, February 1991. http://dx.doi.org/10.21236/ada234991.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Stricker, Lawrence J., and David L. Alderton. Response Latency Measures for Biographical Inventories. Fort Belvoir, VA: Defense Technical Information Center, February 1991. http://dx.doi.org/10.21236/ada235010.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Srinivasan, Srikanth T., and Alvin R. Lebeck. Load Latency Tolerance in Dynamically Scheduled Processors. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada440304.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Prusky, Dov, Noel T. Keen, and Benyamin Jacoby. Regulation of Colletotrichum Gloeosporiodes Latency in Avocado. United States Department of Agriculture, January 1985. http://dx.doi.org/10.32747/1985.7561068.bard.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Bertke, Andrea S. Influence of Herpes Simplex Virus Latency-Associated Transcript (LAT) on the Distribution of Latently Infected Neurons. Fort Belvoir, VA: Defense Technical Information Center, February 2007. http://dx.doi.org/10.21236/ad1013850.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Luzum, Brian, and Axel Nothnagel. Improved UT1 Predictions through Low-Latency VLBI Observations. Fort Belvoir, VA: Defense Technical Information Center, March 2010. http://dx.doi.org/10.21236/ada524037.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Cheng, B. Dynamic Link Exchange Protocol (DLEP) Latency Range Extension. Edited by L. Berger. RFC Editor, March 2020. http://dx.doi.org/10.17487/rfc8757.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Latency' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography