Academic literature on the topic 'LTNP'

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Journal articles on the topic "LTNP"

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Ayala-Suárez, Rubén, Francisco Díez-Fuertes, Esther Calonge, Humberto Erick De La Torre Tarazona, María Gracia-Ruíz de Alda, Laura Capa, and José Alcamí. "Insight in miRNome of Long-Term Non-Progressors and Elite Controllers Exposes Potential RNAi Role in Restraining HIV-1 Infection." Journal of Clinical Medicine 9, no. 8 (July 31, 2020): 2452. http://dx.doi.org/10.3390/jcm9082452.

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Long-term non-progressors (LTNP) and elite controllers (EC) represent spontaneous natural models of efficient HIV-1 response in the absence of treatment. The main purposes of this work are to describe the miRNome of HIV-1 infected patients with different extreme phenotypes and identify potentially altered pathways regulated by differentially expressed (DE) miRNAs. The miRNomes from peripheral blood mononuclear cells (PBMCs) of dual phenotype EC-LTNP or LTNP with detectable viremia and HIV-infected patients with typical progression before and after treatment, were obtained through miRNA-Seq and compared among them. The administration of treatment produces 18 DE miRNAs in typical progressors. LTNP condition shows 14 DE miRNA when compared to typical progressors, allowing LTNP phenotype differentiation. A set of four miRNAs: miR-144-3p, miR-18a-5p, miR-451a, and miR-324 is strongly downregulated in LTNP and related to protein regulation as AKT, mTOR, ERK or IKK, involved in immune response pathways. Deregulation of 28 miRNA is observed between EC-LTNP and viremic-LTNP, including previously described anti-HIV miRNAs: miR-29a, associated with LTNP phenotype, and miR-155, targeting different pre-integration complexes such as ADAM10 and TNPO3. A holistic perspective of the changes observed in the miRNome of patients with different phenotypes of HIV-control and non-progression is provided.
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Swathirajan, Chinnambedu Ravichandran, Ramachandran Vignesh, Greer Waldrop, Uma Shanmugasundaram, Pannerselvam Nandagopal, Sunil Suhas Solomon, Amrose Pradeep, Shanmugam Saravanan, and Kailapuri Gangatharan Murugavel. "HIV-specific T-cell Responses and Generalized Activation in HIV-1 Infected Long-term Non-progressors and Progressors from South India." Current HIV Research 16, no. 4 (January 14, 2019): 302–14. http://dx.doi.org/10.2174/1570162x17666181212122607.

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Background:Anti-viral cytokine expressions by cytotoxic T-cells and lower activation rates have been reported to correlate with suppressed HIV replication in long-term non-progressors (LTNP). Immune mechanisms underlying disease non-progression in LTNP might vary with HIV-1 subtype and geographical locations.Objective:This study evaluates cytokine expression and T-cells activation in relation to disease non-progression in LTNP.Methods:HIV-1 Subtype C infected LTNP (n=20) and progressors (n=15) were enrolled and flowcytometry assays were performed to study HIV-specific CD8 T-cells expressing IL-2, IFN-γ, TNF-α and MIP-1β against gag and env peptides. CD4+ T-cell activation was evaluated by surface expression of HLADR and CD38.Results:Proportions of cytokines studied did not differ significantly between LTNP and progressors, while contrasting correlations with disease progression markers were observed in LTNP. CD4+ T-cell activation rates were significantly lower in LTNP compared to progressors which indicate the potential role of T-cell activation rates in disease non-progression in LTNP.Conclusion:LTNP and progressors showed similar CD8+ T-cell responses, but final conclusions can be drawn only by comparing multiple immune factors in larger LTNP cohort with HIV-1 infected individuals at various levels of disease progression. A possible role of HIV-1 subtype variation and ethnic differences in addition to host-genetic and viral factors cannot be ruled out.
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Michel, Katherine Gisella, Bing Ma, Kathleen Weber, Leah McClellan, Anandi Sheth, Stephen Gange, Audrey French, Jacques Ravel, Igho Ofotokun, and Daniel Merenstein. "4117 UNIQUE VAGINAL MICROBIOME POPULATIONS AND MICROBIAL GENE CONTENT AMONG WOMEN WHO NATURALLY CONTROL HIV PROGRESSION." Journal of Clinical and Translational Science 4, s1 (June 2020): 20–21. http://dx.doi.org/10.1017/cts.2020.102.

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OBJECTIVES/GOALS: The role of the vaginal microbiome (VM) in HIV disease progression is poorly understood. We examined VMs of HIV+ Elite Controllers (ECs) and HIV+ Long-Term Non-Progressors (LTNPs) compared to controls: HIV-positive antiretroviral (ARV) treated (HIV+ATs) and HIV-negative women in the Women’s Interagency HIV Study (DC/Chicago/Atlanta sites). METHODS/STUDY POPULATION: VMs were surveyed via both V3/V4 region of 16S rRNA gene amplicon sequencing and metagenomics sequencing in 67 women across 4 study groups: 1) LTNPs (CD4 >500 cells/mL for 5+ years without ARVs) (n = 7) and 2) ECs (HIV RNA <80 copies/mL for 2+ years without ARVs) (n = 8), matched with 3) HIV+ ATs (on ARVs for ≥1 year with CD4 increase ≥100 cells/mm3) (n = 34), and 4) HIV- women (n = 18). Metagenomes were characterized from specimens collected at two time points: 1) vaginal swabs collected 2016-2017 (n = 62) and 2) cervicovaginal lavage collected 2002-2016 (n = 35; DC/Chicago only). We used VIRGO (human vaginal non-redundant gene catalog), a newly developed referencing framework to comprehensively catalog VM gene content, taxonomy and functions. RESULTS/ANTICIPATED RESULTS: Women were 89% African American with a mean age of 46 years (SD 8.8). The most prevalent species were Gardnerella vaginalis (predominant in 34%), Lactobacillus iners (predominant in 21%), and L. crispatus (predominant in 14%). 90% of LTNP and 45% of EC samples were Lactobacillus-dominant vs. 28% of HIV- and 30% of HIV+ATs. L. crispatus and L. iners in ECs/LTNPs had significantly different gene content and greater gene richness vs. controls. G. vaginalis-predominant communities were found in 66% of HIV- and 68% of HIV+ATs, compared to 46% of EC and 0% of LTNP. The G. vaginalis strains present in EC/LTNP also showed significantly lower gene richness and different gene content vs. controls. DISCUSSION/SIGNIFICANCE OF IMPACT: These results suggest unique VM communities among EC/LTNP, and led us to hypothesize that differential regulation of vaginal immunity drives the observed differences. The similarity between VMs of HIV- and HIV+ATs warrants further study. Larger longitudinal VM studies are needed to assess associated functional pathways and understand the etiology of VM association with HIV progression. CONFLICT OF INTEREST DESCRIPTION: The authors have no conflicts of interest to disclose.
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Panoutsakopoulou, Vily, Kathryn Hunter, Thomas G. Sieck, Elizabeth P. Blankenhorn, and Kenneth J. Blank. "Genetic Regulation of Long-Term Nonprogression in E-55+ Murine Leukemia Virus Infection in Mice." Journal of Virology 73, no. 11 (November 1, 1999): 9232–36. http://dx.doi.org/10.1128/jvi.73.11.9232-9236.1999.

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ABSTRACT Certain inbred mouse strains display progression to lymphoma development after infection with E-55+ murine leukemia virus (E-55+ MuLV), while others demonstrate long-term nonprogression. This difference in disease progression occurs despite the fact that E-55+ MuLV causes persistent infection in both immunocompetent BALB/c–H-2k (BALB.K) progressor (P) and C57BL/10–H-2k (B10.BR) long-term nonprogressor (LTNP) mice. In contrast to immunocompetent mice, immunosuppressed mice from both P and LTNP strains develop lymphomas about 2 months after infection, indicating that the LTNP phenotype is determined by the immune response of the infected mouse. In this study, we used bone marrow chimeras to demonstrate that the LTNP phenotype is associated with the genotype of donor bone marrow and not the recipient microenvironment. In addition, we have mapped a genetic locus that may be responsible for the LTNP trait. Microsatellite-based linkage analysis demonstrated that a non-major histocompatibility complex gene on chromosome 15 regulates long-term survival and is located in the same region as the Rfv3 gene. Rfv3 is involved in recovery from Friend virus-induced leukemia and has been demonstrated to regulate neutralizing virus antibody titers. In our studies, however, both P and LTNP strains produce similar titers of neutralizing and cytotoxic anti-E-55+ MuLV. Therefore, while it is possible that Rfv3 influences the course of E-55+ MuLV infection, it is more likely that the LTNP phenotype in E-55+ MuLV-infected mice is regulated by a different, closely linked gene.
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Pushker, Ravindra, Jean-Marc Jacqué, and Denis C. Shields. "Meta-Analysis To Test the Association of HIV-1 nef Amino Acid Differences and Deletions with Disease Progression." Journal of Virology 84, no. 7 (January 13, 2010): 3644–53. http://dx.doi.org/10.1128/jvi.01959-09.

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ABSTRACT Previous relatively small studies have associated particular amino acid replacements and deletions in the HIV-1 nef gene with differences in the rate of HIV disease progression. We tested more rigorously whether particular nef amino acid differences and deletions are associated with HIV disease progression. Amino acid replacements and deletions in patients' consensus sequences were investigated for 153 progressor (P), 615 long-term nonprogressor (LTNP), and 2,311 unknown progressor sequences from 582 subtype B HIV-infected patients. LTNPs had more defective nefs (interrupted by frameshifts or stop codons), but on a per-patient basis there was no excess of LTNP patients with one or more defective nef sequences compared to the Ps (P = 0.47). The high frequency of amino acid replacement at residues S8, V10, I11, A15, V85, V133, N157, S163, V168, D174, R178, E182, and R188 in LTNPs was also seen in permuted datasets, implying that these are simply rapidly evolving residues. Permutation testing revealed that residues showing the greatest excess over expectation (A15, V85, N157, S163, V168, D174, R178, and R188) were not significant (P = 0.77). Exploratory analysis suggested a hypothetical excess of frameshifting in the regions 9SVIG and 118QGYF among LTNPs. The regions V10 and 152KVEEA of nef were commonly deleted in LTNPs. However, permutation testing indicated that none of the regions displayed significantly excessive deletion in LTNPs. In conclusion, meta-analysis of HIV-1 nef sequences provides no clear evidence of whether defective nef sequences or particular regions of the protein play a significant role in disease progression.
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Broström, Christina, Anders Sönnerborg, Stefan Lindbäck, and Hans Gaines. "Low Relative Frequencies of CD26+CD4+ Cells in Long-Term Nonprogressing Human Immunodeficiency Virus Type 1-Infected Subjects." Clinical Diagnostic Laboratory Immunology 5, no. 5 (September 1, 1998): 662–66. http://dx.doi.org/10.1128/cdli.5.5.662-666.1998.

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ABSTRACT A broad antibody panel was used for immunophenotyping of human immunodeficiency virus type 1 (HIV-1)-infected patients who were long-term nonprogressors (LTNP). The LTNP were compared with patients in the early phase of infection and patients who had progressed to advanced immunodeficiency. Changes in CD8+ subset distribution were observed mainly at acquisition of HIV-1 infection, whereas CD4+ subset changes appeared during progression of HIV-1 infection. The decreasing levels of CD4+ cells were characterized by an increasing frequency of cells expressing the activation markers HLA-Dr and CD45RO but not the CD28 surface antigen. The LTNP exhibited significant changes compared to HIV-negative patients in almost all markers. Compared to patients in the early phase of infection, the only difference was a relatively lower frequency of CD4+ cells expressing CD26 among the LTNP. The results show that HIV-1-infected persons who have no signs of immunodeficiency despite many years of infection have an immunophenotypic pattern that is substantially different from that of noninfected persons. Despite the long duration of infection, the LTNP exhibit a pattern similar to that of newly infected persons, with the exception of lower expression of CD26 on CD4+ cells.
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Ogundeyi, MM, OO Oba-Daini, UP Adeniyi, and BI Adenuga. "A case report A Nigerian adolescent with Long term Non-progressive HIV-infection: A case report." Annals of Health Research 6, no. 2 (May 17, 2020): 239–45. http://dx.doi.org/10.30442/ahr.0602-13-86.

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Children infected with the Human Immunodeficiency Virus (HIV) can be rapid progressors or be at the end of the spectrum of the illness as Long-term Non-progressors (LTNPs). Long term non-progressors are patients who never received Highly Active Anti-Retroviral Therapy (HAART) during the first decade of life and are maintaining good CD4+ count associated with declining HIV RNA values. The literature on paediatric patients with LTNP infection is sparse. An adolescent with HIV LTNP and likely vertical transmission of HIV is presented in this report. She presented with chronic cough, severe anaemia and dyspnea. She was wasted with bodyweight less than the 5th centile for age. She was not sexually active and had no history of blood transfusion, scarification, incisions or sharing of sharp grooming objects. The results of investigations suggested pulmonary tuberculosis and HIV infection. Her CD4 count was 42%. She was commenced on HAART and subsequently, anti-tuberculosis medications according to NTBLCP/DOTS Programme with improvement in symptoms and appreciable weight gain. Therefore routine voluntary HIV testing is recommended for all paediatric admission after consent or assent is obtained bearing in mind that a small subset of patients may fall into the LTNPs population.
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Crotti, Andrea, Francesca Neri, Davide Corti, Silvia Ghezzi, Silvia Heltai, Andreas Baur, Guido Poli, Elena Santagostino, and Elisa Vicenzi. "Nef Alleles from Human Immunodeficiency Virus Type 1-InfectedLong-Term-Nonprogressor Hemophiliacs with or without Late Disease Progression Are Defective in Enhancing Virus Replication and CD4 Down-Regulation." Journal of Virology 80, no. 21 (August 30, 2006): 10663–74. http://dx.doi.org/10.1128/jvi.02621-05.

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ABSTRACT Infection with human immunodeficiency virus (HIV)-encoding defective nef variants may contribute to a relatively benign course of disease in a minority of long-term nonprogressors (LTNP). We have examined the functions of nef alleles from six individuals belonging to the same cohort of hemophiliacs infected with HIV-1 prior to 1985 and classified as LTNP in 1995. Three out of six individuals have progressed to HIV disease (late progressors [LP]), whereas the three remainders have maintained their LTNP status at least up to 2003. The nef alleles were obtained from both plasma virus and peripheral blood mononuclear cells of all six individuals in 1995 and 1998. The proportion of sequences containing mutations not yielding Nef expression significantly diminished in 1998 versus that in 1995. Several previously defined functional regions of intact nef alleles were highly conserved. However, the major variant obtained in 1998 from plasma RNA of five out of six individuals significantly reduced HIV infectivity/replication and impaired Nef-mediated CD4 but not major histocompatibility complex class I antigen down-modulation from the cell surface. Thus, functional alterations of the nef gene are present in both LP and LTNP, suggesting that Nef defectiveness in vitro is not necessarily associated with the long-term maintenance of LTNP status. Of interest is the fact that isolates from three out of three LP showed a dual CCR5/CXCR4 coreceptor use (R5X4), in contrast to those from LTNP, which were exclusively R5. Thus, in vivo evolution of gp120 Env to CXCR4 use appears to be associated with HIV disease progression in individuals infected with nef-defective viruses.
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Gaardbo, Julie C., Hans J. Hartling, Jan Gerstoft, and Susanne D. Nielsen. "Thirty Years with HIV Infection—Nonprogression Is Still Puzzling: Lessons to Be Learned from Controllers and Long-Term Nonprogressors." AIDS Research and Treatment 2012 (2012): 1–14. http://dx.doi.org/10.1155/2012/161584.

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In the early days of the HIV epidemic, it was observed that a minority of the infected patients did not progress to AIDS or death and maintained stable CD4+ cell counts. As the technique for measuring viral load became available it was evident that some of these nonprogressors in addition to preserved CD4+ cell counts had very low or even undetectable viral replication. They were therefore termed controllers, while those with viral replication were termed long-term nonprogressors (LTNPs). Genetics and virology play a role in nonprogression, but does not provide a full explanation. Therefore, host differences in the immunological response have been proposed. Moreover, the immunological response can be divided into an immune homeostasis resistant to HIV and an immune response leading to viral control. Thus, non-progression in LTNP and controllers may be due to different immunological mechanisms. Understanding the lack of disease progression and the different interactions between HIV and the immune system could ideally teach us how to develop a functional cure for HIV infection. Here we review immunological features of controllers and LTNP, highlighting differences and clinical implications.
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Lefrère, Jean-Jacques, Laurence Morand-Joubert, Martine Mariotti, Hubertus Bludau, Béatrice Burghoffer, Jean-Claude Petit, and Françoise Roudot-Thoraval. "Even Individuals Considered as Long-Term Nonprogressors Show Biological Signs of Progression After 10 Years of Human Immunodeficiency Virus Infection." Blood 90, no. 3 (August 1, 1997): 1133–40. http://dx.doi.org/10.1182/blood.v90.3.1133.

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Abstract Despite a decade of human immunodeficiency virus (HIV) seropositivity, a few individuals termed as long-term nonprogressors (LTNPs) maintain a stable CD4+ T-cell count for a period of time. The aim of this study was to establish, through the sequential determination of all known predictors of HIV disease, the proportion of such patients having stringent criteria of true long-term nonprogression. Among 249 individuals who were HIV-infected and prospectively followed up over a 10-year period (1985 to 1995), 12 having a CD4+ T-cell count greater than 500/μL (LTNP I group) and 9 having a CD4+ T-cell count less than 500 but stable over time (LTNP II group) after at least 10 years of infection without intervention of antiviral therapy, were studied over the entire follow-up period. The plasma HIV RNA copy number and the serum concentrations of p24 antigen, each anti-HIV antibody, neopterin, β-2-microglobulin, Immunoglobulin (Ig) G and IgA were determined every 18 months over the study period. Cellular and plasma viremias were cross-sectionaly assayed in all 21 patients. Only two patients had strictly no marker of progression over the follow-up period. They were the only ones who had, over the 10-year period, a viral copy number too low to be detected. The other patients had a viral copy number higher than 400/mL at at least one visit and increasing over the follow-up period, and they evidenced one or more markers of virological or immunological deterioration. Cellular viremia was positive in all patients but two, while plasma viremia was negative in all but one. The population of individuals termed as LTNPs is not virologically and immunologically homogeneous. The majority present biological signs of HIV disease progression. A new pattern of true LTNP can be drawn through stringent criteria based on the whole known predictors. This pattern appears to be rare in HIV-positive population.
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Dissertations / Theses on the topic "LTNP"

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Conceicao, Viviane. "Genome-Wide Host Gene Expression Analysis Before and After the Initiation of Highly Active Antiretroviral Therapy And Natural Control of HIV in Therapy Naïve HIV+ Non-Progressors." Thesis, The University of Sydney, 2013. http://hdl.handle.net/2123/9384.

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Since its discovery 25 years ago, the HIV virus has infected more than 34 million people in the world; the infection caused by this virus has led the world to its most terrible pandemic, and the greatest global health crises of our times. The host-virus interaction and natural history of the disease are influenced by the distinctive interface the virus has with each infected individual. The infection with HIV-1 is characterized by the destruction of CD4+ T-cells during the typical course of the infection, but HIV has the arsenal to infect practically all the major blood leukocytes. Taken from these observations, it is apparent that HIV has the innate ability to subvert and manipulate the host gene machinery at the transcriptomic level. The highly active anti-retroviral therapy (HAART) consists of a combination of powerful drugs, which serve as potent defence mechanism against the ways in which the HIV virus attacks the human bod y. Although these drugs are not able to rid the body of HIV virus, they can significantly delay the onset of AIDS and reduce the incidence of opportunistic infections, morbidity and mortality related to HIV infection. After the introduction of HAART treatment, it is observed that most patients with good adherence respond to HAART, which is defined by a decrease of plasma viral load to undetectable levels and an immune reconstitution with a significant increase of CD4+ T cell levels. Around 30% of the patients fail to achieve this response and continue to express high plasma viral load and low CD4+ T cell numbers. In contrast, some rare HIV+ patients maintain below detectable levels of plasma viremia without the treatment. These are termed long-term nonprogressors(LTNPs), less commonly called elite controllers. These rare individuals are infected with HIV, but have the natural ability to control the infection with the strength of their immune system. Many of th ese patients have been HIV positive for 30 years or more and! off the rapy for the entire duration of their infection, showing high CD4+T cells counts and no progression to the disease. In this context, it is important to mention that the genomic basis of this natural effective immunological control of viremia in LTNPs, as opposed to drug-mediated control of HIV, remains unknown. The development of high throughput microarray platforms and bioinformatic platforms to visualize and analyse the complex dataset has enabled considerable progress in the field of viral genomics, and also the visualization of host-virus interactions at the molecular level. In chapter III, we carried out a comparative genome-wide (encompassing all 25,000 human genes) pharmacogenomic study using whole primary peripheral blood mononuclear cells (PBMC) derived from 14 HIV+ patients at two time points: pre-HAART (TP-1 with detectable viremia) and post (TP2: below detectable level (BDL) of plasma HIV <40 copies of HIV RNA/mL plasma), to ascertain how genomically distinct viremic phase is from the phase in which virus is fully controlled with HAART. Another goal was to define the underlying pharmacogenomic basis of HIV control during HAART. In the second study shown in Chapter IV, we compared the two time points against the 9 LTNPs to unravel the genomic basis of natural control of viremia in therapy naïve LTNPs showing below detectable levels of viremia (<20 copies of HIV RNA/mL plasma) and high and stable CD4+T cell counts. Genomic RNA extracted from the PBMCs was used in genome-wide microarray analysis, using HT-12v3 Illumina chips. Quantile normalization was performed to normalize the data and inter-patient variability. Illumina®BeadStudio Data Analysis Software wa s used to obtain differentially expressed (DE) genes. Only the significant genes with p value <0.01 and FDR of <5% (for the comparison between TP1 and TP2) and FDR <1% (for the comparison between LTNP vers us TP1 and LTNP versus TP2) were considered appropriate for ! analysis . Pathway analysis was performed in MetaCoreTM from GeneGo, Inc to derive functional annotations. Functionally significant genes were validated by quantitative real time PCR. Between TP1 and TP2, 234 genes were differentially expressed. Within these genes, 212 were down-regulated and 22 upregulated. Between the comparison between LTNP vs TP1, 965 genes were differently expressed (706 genes were up-regulated and 259 genes were down-regulated), and when LTNP was compared to the TP2 group, we found 1181 DE genes (with 727 genes up-regulated and 454 genes downregulated). In the first part of this study, comparing the TP1 and TP2 only, we found that of the top 10 pathways, 8 belonged to the immune response system. This was the most significant pathway up-regulated in TP1 when compared to TP2. This comprised of genes that were involved in antiviral action of interferon (IFN) and their signalling function, antiviral response, dendritic cell maturation a nd migration, and cell metabolism. Map folder and enrichment analysis corroborated with our findings, thereby confirming an intrinsic role of the immune, inflammatory and interferon response family-related genes during HIV viremia in the absence of treatment. But a closer examination of this contrast also showed a mirror down-regulation of genes involved in innate and adaptive immunity, inflammation, apoptosis and antiviral functions. This directly implies a functional relevance of these pathways, through their modulation in TP1 and TP2 stages. Although these data are intuitive and expected, such analysis has never been performed before. The second part of this study, on comparisons between LTNP and TP1 and LTNP against TP2, we show the first evidence demonstrating that the natural control of HIV in LTNP is guided by the genes enriched in the immune response, cytoskeleton remodelling, apoptosis and T cell signalling pathways. Another striking ob servation was that, even though the LTNP and TP2 groups maintai ned BDL of plasma viremia (<40 copies), the LTNP group was genomically distinct from the TP2, which controlled viremia with HAART. This highlights the qualitative distinction and critical role of enriched pathways in natural control of viremia in the LTNPs. Seventeen genes encompassing all these pathways were validated by q-PCR, which showed consistent trends between microarray and q-RT PCR. One gene in particular, the thrombospondin (THBS1) (R2= 0.942) was identified as a biomarker in our study, discriminating between viremic patients and LTNPs at the genomic (R2= 0.942, p<2.654e.08) and proteomic levels (p<0.003761). The levels of expression of THBS1 showed excellent correlation with plasma viremia (R2=0.81557;p<.0.0003761), the first description of such an important protein. This is the most unique finding of this work, which has significance in HIV disease prognostics and diagnostics, in addition to predicting the strength of the ho st immune system, as evident from its down-regulation and low expression in the natural controllers. Overall, through these analyses, we have shown that, although there are common set of key genes associated with HIV at all stages, each stage also showed unique molecular signatures. This was demonstrated with the identification of molecular signatures for the control of virus with HAART therapy, as well as for the natural control of HIV in LTNPs. Especially for the LTNPs, the downregulation of the apoptosis was the most significant feature, which may have important implications in therapy, especially in the context of using apoptosis as a target for future therapies.
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van, Bockel David John Clinical School St Vincent's Hospital Faculty of Medicine UNSW. "Qualitative analysis of T-cell repertoire for relevance to non-progressive HIV infection." Publisher:University of New South Wales. Clinical School - St Vincent's Hospital, 2008. http://handle.unsw.edu.au/1959.4/41304.

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Cytotoxic T-lymphocytes are important for the control of viral replication during HIV infection, however the magnitude and breadth of HIV-specific CD8+ T-cell response does not correlate well. The purpose for this study was the examination of the HLA-B*2705-specific CD8+ T-cell response to the KRWIILGLNK (KK10) epitope as a definitive model of immune control over HIV replication. The breadth of the T-cell receptor (TCR) repertoire was determined for an association between the qualitative nature of this response and immune escape and therefore, disease progression. Methodology was developed and validated for TCR repertoire analysis in formaldehyde fixed antigen-specific CD8+ T-cells. The TCR repertoire for the KK10-specific CD8+ T-cell response was defined in cross-section and longitudinally for 6 HLA-B*2705+ patients. Comparison was made to cognate HLA-A*0201 CMV NV9 and HLA-B*2705 EBV RL9-specific CD8+ T-cell populations using the Simpson??s diversity index and the Morisita-Horn similarity index for standardized repertoire analysis. HLA-B*2705 KK10-specific TCR repertoire was not found to be a determinant of control. Greater clonotype variation was found within CMV-specific CD8+ T-cell populations, suggesting an association with reactivation of CMV and disease state. An association was found between KK10-specific population diversity and the prevalence of cognate KK10 epitope in vivo. Cross-reactivity observed for dominant KK10-specific clonotypes suggested that avidity of CD8+ T-cells was important for in vivo survival. Phenotype and function was tested through multiparameter analysis of HIV and CMV-specific CD8+ T-cells. Increased frequency of CD127 (IL-7R) and Bcl-2 expression within dominant populations was suggestive of selective advantage. Division of dominant and sub-dominant CMV-specific CD8+ T-cell populations into ??early?? and ??late?? differentiation phenotypes indicated virus-specific mechanisms of clonotype turn over. No simple association of TCR expression was found for HIV and CMV-specific CD8+ T-cells with published examples of definitive TCR bias. Over-represented TCR ??-chain families of patients were found in association with public clonotypes. Convergent recombination of TCR genes was demonstrated as a mechanism for the prevalence of shared clonotypes. Standardized assessment of T-cell repertoire successfully identified mechanisms of antigen-specific CD8+ T-cell recruitment. A substantial increase in sample numbers is required before this methodology can be used to accurately demonstrate the importance of TCR repertoire usage in the control of human viral infection.
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Bignami, F. "L'ESPOSIZIONE AD HIV-1 INFLUENZA LA RISPOSTA IMMUNITARIA CD4-MEDIATA ALTERANDO IL PROFILO D'ESPRESSIONE DEI MICRORNA CELLULARI." Doctoral thesis, Università degli Studi di Milano, 2010. http://hdl.handle.net/2434/150033.

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MicroRNAs (miRNAs) are small single-strand non-coding RNAs that repress gene expression by inhibiting translation. MiRNAs are known to inhibit HIV-1 expression interfering with viral mRNAs. In order to better understand how HIV-related alterations in cellular physiology and immunologic control function, 3 classes of patients (éLTNP, Naive and multiply exposed to HIV-1 uninfected subjects, named MEU) were enrolled, from whom blood CD4+ cells were purified. In this cellular subtype the expression levels of 377 miRNAs were analyzed by TaqMan real-time PCR-based arrays. Only miRNAs expressed in 70% of patients of at least one class and of at least 1 log10 variation from healthy controls were selected. A similar analysis had also been performed in primary culture of CD4+T cells and monocyte-macrophages infected by R5 strains and in CD4+ cells exposed to recombinant and natural gp120 molecules in vitro. In all experiments, expression levels of Dicer and Drosha, two enzymes involved in miRNA biogenesis, were evaluated by real-time PCR. Similar miRNA profiles were detected in the CD4+ cells from éLTNP and Naive, although these infected patients had different parameters such as viral and proviral loads, infection time and CD4+ T cell number. Moreover, a complex down-regulation of miRNA was observed in the CD4+ cells from MEU subjects. This indicates that the only HIV-1 antigen exposure can modulate cellular programming process of CD4+ cells. Three up-regulated (miR-203, 449a, 502-5p) and five down-regulated (miR-329, 337-5p, 379, 503, 518d-3p) miRNAs, modulated in all patient classes, defined a HIV-1 signature. By hierarchical clustering of the miRNA profile, éLTNP clustered with Naive patients, whereas all MEU subjects grouped together; this suggests that miRNA expression may discriminate between infected and uninfected individuals. By statistical analysis, 16 miRNAs significantly differentiated éLTNP and Naive from MEU, while only the miR-155 discriminated éLTNP from Naive. Of these, 9 were involved in viral replication and/or in immune response. Computational studies suggested that target genes of altered miRNAs are involved in a lot of cellular processes and in binding/catalytic activity. According to the Dicer and Drosha expression, that was down-regulated in all patient classes, a correlation was observed between miRNA and the two enzymes expression. In contrast, no differences were observed in CD4+ cells infected in vitro or exposed to gp120 molecules. This suggests that there is a complex regulation of miRNA expression after HIV exposure, not only due to the miRNA biogenesis. The miRNA expression analysis in CD4+ cells exposed to gp120 molecules showed a modulation of 66 miRNAs; only 42% of these showed the same levels of expression, suggesting that the remaining percentage of miRNAs was modulated by other gp120 epitopes. When the gp120 was neutralized with mAbs, only 1/3 of altered miRNAs were reverted to the expression of non exposed controls. This indicates the existence of epitopes (other than the CD4 binding domain) capable of inducing a miRNA modulation. Finally, the miRNA expression analysis highlights that 5 miRNAs (miR-34c-p, 518f, 452, 202 and 487b) could have a role in HIV-CD4+ cell binding. In conclusion, in light of these results, it can be supposed that the altered miRNA profile is due to the constant HIV exposure of CD4+ cells through a bystander phenomenon rather than a direct effect. Therefore it can be assumed that only the exposure to gp120 molecules can leave a signature in immune cells.
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Parnicza, Justin W. "WV LTAP PMS integrating GIS with PMS software /." Morgantown, W. Va. : [West Virginia University Libraries], 2010. http://hdl.handle.net/10450/10848.

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Thesis (M.S.)--West Virginia University, 2010.
Title from document title page. Document formatted into pages; contains ix, 97 p. : ill. (some col.), col. maps. Includes abstract. Includes bibliographical references (p. 51).
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Arend, Marcos Osmar. "Lente Toroidal de Plasma (LTP)." Pontif?cia Universidade Cat?lica do Rio Grande do Sul, 2016. http://tede2.pucrs.br/tede2/handle/tede/7003.

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This paper proposes the use of plasma lenses to replace the classical solid dielectric lens for focusing the electromagnetic wave, with application in theaters of military operations. The results are shown for an array of plasma elements constituting a directional antenna with innovative features. One of the major advantages is the reduced cross section presented to the electromagnetic wave emitted by a radar system, minimizing the detection probability in specific operational bands, thus maximizing the invisibility of the proposed system.
Este trabalho prop?e o uso de lentes de plasma em substitui??o ? cl?ssica lente diel?trica s?lida para focaliza??o de ondas-eletromagn?ticas, com aplica??o em teatros de opera??es militares. Os resultados s?o demonstrados em um arranjo de elementos de plasma, constituindo uma antena direcional de aracter?sticas inovadoras. Um dos principais diferenciais se refere ? reduzida se??o transversal apresentada ? onda eletromagn?tica emitida por sistemas de radar (RCS), minimizando em determinadas bandas de opera??o a probabilidade de detec??o, maximizando, portanto, a invisibilidade do sistema proposto.
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Lack, Jeremy David. "The solution structure and surface properties of TB3 of LTBP-1." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249190.

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Steer, Ruth. "Investigations of the extracellular deposition of latent TGF-beta binding protein-1 (LTBP-1)." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/investigations-of-the-extracellular-deposition-of-latent-tgfbeta-binding-protein1-ltbp1(41e0ee4f-5030-4333-8a52-e0d21d1fc649).html.

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LTBP-1 is a large extracellular glycoprotein that is a component of the large latent TGF-β complex. The extracellular sequestration of latent TGF-β in the extracellular matrix (ECM) is fundamental to the regulation of TGF-β bioavailability and activity. LTBP-1 is described to contribute to the regulation of TGF-β bioavailability through mediating the extracellular sequestration of newly secreted latent TGF-β with fibrillin microfibrils in the ECM. However it is not well understood how LTBP-1, and thus latent TGF-β, becomes deposited into the ECM. Previous work by our group suggested that LTBP-1 interactions with the glycosaminoglycan heparan sulphate (HS) at the cell-matrix interface might facilitate the association of LTBP-1 with fibrillin microfibrils. Using recombinant LTBP-1 fragments and mutants, LTBP-1 interaction with HS have been fine-mapped. Deposition of a LTBP-1 HS-binding mutant, and of LTBP-1 when HS was depleted, was studied in cell cultures; findings presented here demonstrate that HS may not be critical for the deposition of LTBP-1 into the ECM. Contributions of fibrillin and fibronectin to LTBP-1 deposition were investigated, and data presented here support published findings that fibrillin is not always required for LTBP-1 deposition. In addition, the dependency of LTBP-1 deposition upon fibronectin was suggested to differ between different cell types (epithelial and mesenchymal). How LTBP-1 may be stabilised within the ECM through crosslinking by tissue transglutaminase was investigated using recombinant fragments and cell culture studies. Tissue transglutaminase was found to promote the extracellular incorporation of LTBP-1, and novel cross-links within LTBP-1, and between LTBP-1 and fibrillin-1, but not LTBP-1 and fibronectin, were identified. Additionally, results indicated that LTBP-1 was present in extremely high molecular weight assemblies in the ECM of cultured fibroblasts. Collectively, these results have contributed to current knowledge of how LTBP-1 becomes deposited into the ECM. They indicate that the deposition of LTBP-1 is not underpinned by HS, may be cell type-specific, and that LTBP-1 may potentially self-assemble extracellularly into homotypic structures that may associate with fibrillin microfibrils.
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Evans, Gary Lee. "The induction of long-term potentiation attenuates kainic acid-induced excitotoxicity." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/777.

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The activation of N-methyl-D-aspartate glutamate receptors (NMDARs) is required for the long term potentiation (LTP) and long term depression (LTD) of excitatory synaptic transmission at hippocampal CA1 synapses, and plays an important role in learning and memory. In addition, it is accepted that the over-activation of NMDARs leads to the neurotoxicity associated with stroke and other neurodegenerative disorders. Thus, the NMDAR provides a logical starting point to investigate a possible relationship between synaptic plasticity and the cell-signalling pathways which ultimately determine neuronal fate. Research in our lab has indicated that NR2A-containing NMDARs are essential for LTP induction whereas NR2B-containing NMDARs are crucial for the production of LTD in vitro, and the results of this study support these findings in the anaesthetized rat. Furthermore, using the kainic acid (KA) model of neurotoxicity, this research has explored the opposing roles that activity-dependent synaptic plasticity, through different NMDAR subtypes, can play in determining neuronal outcome in an excitotoxic environment. In these experiments, it is shown that (1) the induction of LTP using high-frequency stimulation (HFS) promotes the phosphorylation of Akt, which plays a critical role in controlling cell survival and apoptosis, (2) the induction of LTP using HFS attenuates kainic acid (KA) induced neurodegeneration while the induction of LTD using low-frequency stimulation (LFS) has no incremental effect on the degree of cell death resulting from exposure to KA, (3) the blockade of NR2B-containing NMDARs using Ro25-6981 attenuates KA-induced neurodegeneration while the blockade of NR2A-containing NMDARs using NVP-AAM077 does not influence KA-induced neurotoxicity, (4) pre-treatment with NR2A antagonists blocks both the induction of LTP and its neuroprotective effect against KA while NR2B antagonists neither block the induction of LTP nor the neuroprotection that this can provide against KA, (5) the administration of NR2A antagonists after the induction of LTP has no effect on the expression of LTP or its neuroprotective effect against KA, and (6) pre-treatment with a high dose (2.4mg/kg) of NVP-AAM077 leads to the induction of LTD rather than LTP as a result of HFS. Altogether this research supports the hypothesis that the production of LTP via the activation of NR2A-containing NMDARs protects neurons against excitotoxic neuronal death by promoting cell survival signalling. Furthermore, because NR2A antagonists applied after the production of LTP do not block neuroprotection, it can be concluded that LTP itself, and not NR2A activation, is responsible for this neuroprotective effect.
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Yan, Yi. "The role of Akt in AMPA receptor insertion and LTP." Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/31741.

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It has been widely accepted that long-term potentiation (LTP) in the hippocampal CA1 region mostly results from increased insertion of post-synaptic α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptors (AMPARs). The previous study in our lab has shown that activation of phosphatidylinositol 3-kinase (PI3K) by selective stimulation of synaptic N-methyl-D-aspartate receptors (NMDARs) is required for the increased cell surface expression of AMPARs and the consequent LTP. However, the following signaling pathways still remain unknown. In the present study, the involvement of Akt, the primary downstream protein kinase of PI3K, was examined with a combination of electrophysiological, biochemical and molecular biological techniques. The study found that Akt is required for the post-synaptic AMPAR insertion and LTP. Furthermore, the threonine 840 (Thr840) on GluRl C-tail was identified as a novel Akt phosphorylation site, suggesting a potential mechanism by which Akt contributes to AMPAR incorporation and LTP.
Medicine, Faculty of
Graduate
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Lu, You Ming. "Signaling cascades underlying two different forms of LTP in hippocampus." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0007/NQ41219.pdf.

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Books on the topic "LTNP"

1

Evans, Lynn D. LTPP profile variability. McLean, Va: U.S. Dept. of Transportation, Federal Highway Administration, Research, Development, and Technology, Turner-Fairbank Highway Research Center, 2000.

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United States. Federal Highway Administration., ed. LTPP product plan. [McLean, Va.?]: U.S. Dept. of Transportation, Federal Highway Administration, 2001.

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United States. Federal Highway Administration., ed. LTPP product plan. [McLean, Va.?]: U.S. Dept. of Transportation, Federal Highway Administration, 2001.

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author, Frangopol Dan M., and United States. Federal Highway Administration. Offices of Research, Development, and Technology, eds. LTBP bridge performance primer. McLean, VA: U.S. Department of Transportation, Federal Highway Administration, Research, Development and Technology, Turner-Fairbank Highway Research Center, 2013.

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United States. Federal Highway Administration., ed. LTPP, the next decade. [Washington, D.C.]: U.S. Dept. of Transportation, Federal Highway Administration, 1998.

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Center, Turner-Fairbank Highway Research, ed. LTPP data analysis: Frequently asked questions about joint faulting with answers from LTPP. McLean, VA (6300 Georgetown Pike, McLean 22101-2296): U.S. Dept. of Transportation, Federal Highway Administration, Research and Development, Turner-Fairbank Highway Research Center, 1997.

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Center, Turner-Fairbank Highway Research, ed. LTPP data analysis: Frequently asked questions about joint faulting with answers from LTPP. McLean, VA (6300 Georgetown Pike, McLean 22101-2296): U.S. Dept. of Transportation, Federal Highway Administration, Research and Development, Turner-Fairbank Highway Research Center, 1997.

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LTPP computed parameter: Dynamic modulus. McLean, VA: U.S. Dept. of Transportation, Federal Highway Administration, Research, Development, and Technology, Turner-Fairbank Highway Research Center, 2011.

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United States. Federal Highway Administration., ed. LTTP: Year in review : 2000. [Washington, D.C.]: Federal Highway Administration, 2001.

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United States. Federal Highway Administration., ed. LTPP: 1999 year in review. [Washington, D.C.]: U.S. Dept. of Transportation, Federal Highway Administration, 2000.

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Book chapters on the topic "LTNP"

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Fischer, Gabriele, Annemarie Unger, W. Wolfgang Fleischhacker, Cécile Viollet, Jacques Epelbaum, Daniel Hoyer, Ina Weiner, et al. "LTP." In Encyclopedia of Psychopharmacology, 730. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_4333.

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Straughan, Brian. "Thermal Convection with LTNE." In Advances in Mechanics and Mathematics, 49–68. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-13530-4_2.

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Straughan, Brian. "Rotating Convection with LTNE." In Advances in Mechanics and Mathematics, 69–78. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-13530-4_3.

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Straughan, Brian. "Penetrative Convection with LTNE." In Advances in Mechanics and Mathematics, 95–102. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-13530-4_6.

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Straughan, Brian. "LTNE and Multi-layers." In Advances in Mechanics and Mathematics, 103–11. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-13530-4_7.

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Straughan, Brian. "Double Diffusive Convection with LTNE." In Advances in Mechanics and Mathematics, 79–86. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-13530-4_4.

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Straughan, Brian. "Vertical Porous Convection with LTNE." In Advances in Mechanics and Mathematics, 87–93. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-13530-4_5.

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Staniec, Kamil. "Propagation Models for LTN Systems." In Radio Interfaces in the Internet of Things Systems, 61–77. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44846-2_3.

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Staniec, Kamil. "Radio Interfaces in LTN Networks." In Radio Interfaces in the Internet of Things Systems, 79–92. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44846-2_4.

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Arlein, Robert, Juliana Freire, Narain Gehani, Daniel Lieuwen, and Joann Ordille. "Making LDAP Active with the LTAP Gateway." In Databases in Telecommunications, 54–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/10721056_5.

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Conference papers on the topic "LTNP"

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Poehler, Jeffrey C., Gary L. Stevens, Anees A. Udyawar, and Amy Freed. "Background on Low Temperature Overpressure Protection System Setpoints for Pressure-Temperature Curves." In ASME 2020 Pressure Vessels & Piping Conference. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/pvp2020-21663.

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Abstract ASME Code, Section XI, Nonmandatory Appendix G (ASME-G) provides a methodology for determining pressure and temperature (P-T) limits to prevent non-ductile failure of nuclear reactor pressure vessels (RPVs). Low-Temperature Overpressure Protection (LTOP) refers to systems in nuclear power plants that are designed to prevent inadvertent challenges to the established P-T limits due to operational events such as unexpected mass or temperature additions to the reactor coolant system (RCS). These systems were generally added to commercial nuclear power plants in the 1970s and 1980s to address regulatory concerns related to LTOP events. LTOP systems typically limit the allowable system pressure to below a certain value during plant operation below the LTOP system enabling temperature. Major overpressurization of the RCS, if combined with a critical size crack, could result in a brittle failure of the RPV. Failure of the RPV could make it impossible to provide adequate coolant to the reactor core and result in a major core damage or core melt accident. This issue affected the design and operation of all pressurized water reactors (PWRs). This paper provides a description of an investigation and technical evaluation regarding LTOP setpoints that was performed to review the basis of ASME-G, Paragraph G-2215, “Allowable Pressure,” which includes provisions to address pressure and temperature limitations in the development of P-T curves that incorporate LTOP limits. First, high-level summaries of the LTOP issue and its resolution are provided. LTOP was a significant issue for pressurized water reactors (PWRs) starting in the 1970s, and there are many reports available within the U.S. Nuclear Regulatory Commission’s (NRC’s) documentation system for this topic, including Information Notices, Generic Letters, and NUREGs. Second, a particular aspect of LTOP as related to ASME-G requirements for LTOP is discussed. Lastly, a basis is provided to update Appendix G-2215 to state that LTOP setpoints are based on isothermal (steady-state) conditions. This paper was developed as part of a larger effort to document the technical bases behind ASME-G.
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Muhammad, Fahad Syed, Laurent Franck, and Stephen Farrell. "Transmission protocols for challenging networks: LTP and LTP-T." In 2007 International Workshop on Satellite and Space Communications. IEEE, 2007. http://dx.doi.org/10.1109/iwssc.2007.4409406.

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Buonomo, Bernardo, Davide Ercole, Oronzio Manca, and Sergio Nardini. "Numerical Investigation on a Latent Thermal Energy Storage With Aluminum Foam." In ASME 2016 Heat Transfer Summer Conference collocated with the ASME 2016 Fluids Engineering Division Summer Meeting and the ASME 2016 14th International Conference on Nanochannels, Microchannels, and Minichannels. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/ht2016-7255.

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In this paper, a numerical investigation on Latent Heat Thermal Energy Storage System (LHTESS) based on a phase change material (PCM) in a metal foam is accomplished. A vertical shell and tube LHTESS made with two concentric aluminum tubes is investigated. The internal surface of the hollow cylinder is at a constant temperature above the PCM melting temperature to simulate the heat transfer from a hot fluid. The other external surfaces are assumed adiabatic. The phase change of the PCM is modeled with the enthalpy porosity theory while the metal foam is considered as a porous media that obeys to the Darcy-Forchheimer law. Local thermal non-equilibrium (LTNE) model is assumed to analyze the metal foam and some comparison are accomplished with the local thermal equilibrium model assumption. The governing equations are solved employing the Ansys-Fluent 15 code. Numerical simulations for PCM, PCM in the porous medium in LTE and in LTNE assumptions are obtained. Results as a function of time for the charging phase are carried out for different porosities and assigned pore per inch (PPI). The results show that at high porosity the LTE and LTNE models have the same melting time while at low porosity the LTNE has a larger melting time. Moreover, the presence of metal foam improves significantly the heat transfer in the LHTESS giving a very faster phase change process with respect to pure PCM, reducing the melting time more than one order of magnitude.
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Gururajan, Vyaas, Riccardo Scarcelli, Sayan Biswas, and Isaac Ekoto. "CFD Modeling of Low Temperature Ignition Processes From a Nanosecond Pulsed Discharge at Quiescent Conditions." In ASME 2021 Internal Combustion Engine Division Fall Technical Conference. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/icef2021-67902.

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Abstract Recent interest in non-equilibrium plasma discharges as sources of ignition for the automotive industry has not yet been accompanied by the availability of dedicated models to perform this task in computational fluid dynamics (CFD) engine simulations. The need for a low-temperature plasma (LTP) ignition model has motivated much work in simulating these discharges from first principles. Most ignition models assume that an equilibrium plasma comprises the bulk of discharge kernels. LTP discharges, however, exhibit highly non-equilibrium behavior. In this work, a method to determine a consistent initialization of LTP discharge kernels for use in engine CFD codes like CONVERGE is proposed. The method utilizes first principles discharge simulations. Such an LTP kernel is introduced in a flammable mixture of air and fuel, and the subsequent plasma expansion and ignition simulation is carried out using a reacting flow solver with detailed chemistry. The proposed numerical approach is shown to produce results that agree with experimental observations regarding the ignitability of methane-air and ethylene-air mixtures by LTP discharges.
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Allen, Matthew S. "Floquet Experimental Modal Analysis for System Identification of Linear Time-Periodic Systems." In ASME 2007 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2007. http://dx.doi.org/10.1115/detc2007-34790.

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A variety of systems can be faithfully modeled as linear with coefficients that vary periodically with time or Linear Time-Periodic (LTP). Examples include anisotropic rotorbearing systems, wind turbines, satellite systems, etc… A number of powerful techniques have been presented in the past few decades, so that one might expect to model or control an LTP system with relative ease compared to time varying systems in general. However, few, if any, methods exist for experimentally characterizing LTP systems. This work seeks to produce a set of tools that can be used to characterize LTP systems completely through experiment. While such an approach is commonplace for LTI systems, all current methods for time varying systems require either that the system parameters vary slowly with time or else simply identify a few parameters of a pre-defined model to response data. A previous work presented two methods by which system identification techniques for linear time invariant (LTI) systems could be used to identify a response model for an LTP system from free response data. One of these allows the system’s model order to be determined exactly as if the system were linear time-invariant. This work presents a means whereby the response model identified in the previous work can be used to generate the full state transition matrix and the underlying time varying state matrix from an identified LTP response model and illustrates the entire system-identification process using simulated response data for a Jeffcott rotor in anisotropic bearings.
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Barr, Paul J., Marvin W. Halling, Tommy E. Cousins, Carin L. Roberts-Wollmann, and Elisa D. Sotelino. "LTBP Bridge Monitoring, Testing, and Instrumentation." In Structures Congress 2009. Reston, VA: American Society of Civil Engineers, 2009. http://dx.doi.org/10.1061/41031(341)48.

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Khashan, S. A. "Local Thermal Non-Equilibrium Effect in Forced Convection of Non-Newtonian Fluids Through Porous Media." In ASME 2004 Heat Transfer/Fluids Engineering Summer Conference. ASMEDC, 2004. http://dx.doi.org/10.1115/ht-fed2004-56649.

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In this paper, we examine the effect of local thermal non-equilibrium LTNE condition on the non-Newtonian forced convection flow through channels filled with porous media. Four representative dimensionless parameters are used in formulating the problem. Numerical solutions obtained over broad ranges of these parameters are utilized to map conditions at which local thermal non-equilibrium condition is important, occurrence of LTNE is found to be driven by higher modified Peclet number, lower modified Biot number, lower fluid-to-solid thermal conductivity ratio, lower power-law fluid index, and lower microscopic and macroscopic frictional flow resistance coefficients. The proportional effect of each parameter as related to others is investigated.
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Sembrant, Andreas, Trevor Carlson, Erik Hagersten, David Black-Shaffer, Arthur Perais, André Seznec, and Pierre Michaud. "Long term parking (LTP)." In MICRO-48: The 48th Annual IEEE/ACM International Symposium of Microarchitecture. New York, NY, USA: ACM, 2015. http://dx.doi.org/10.1145/2830772.2830815.

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Buonomo, Bernardo, Davide Ercole, Oronzio Manca, Hasan Celik, and Moghtada Mobedi. "Numerical Investigation on the Effect of Aluminum Foam in a Latent Thermal Energy Storage." In ASME 2015 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/imece2015-53180.

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In this paper, a numerical investigation on Latent Heat Thermal Energy Storage System (LHTESS) based on a phase change material (PCM) is accomplished. The geometry of the system under investigation is a vertical shell and tube LHTES made with two concentric aluminum tubes. The internal surface of the hollow cylinder is assumed at a constant temperature above the melting temperature of the PCM to simulate the heat transfer from a hot fluid. The other external surfaces are assumed adiabatic. The phase change of the PCM is modeled with the enthalpy porosity theory while the metal foam is considered as a porous media that obeys to the Darcy-Forchheimer law. The momentum equations are modified by adding of suitable source term which it allows to model the solid phase of PCM and natural convection in the liquid phase of PCM. Both local thermal equilibrium (LTE) and local thermal non-equilibrium (LTNE) models are examined. Results as a function of time for the charging phase are carried out for different porosities and assigned pore per inch (PPI). The results show that at high porosity the LTE and LTNE models have the same melting time while at low porosity the LTNE has a larger melting time. Moreover, the presence of metal foam improves significantly the heat transfer in the LHTES giving a very faster phase change process with respect to pure PCM, reducing the melting time more than one order of magnitude.
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Hwang, J. J. "Heat Transfer in a Porous Cathode of Fuel Cells." In ASME 2005 Summer Heat Transfer Conference collocated with the ASME 2005 Pacific Rim Technical Conference and Exhibition on Integration and Packaging of MEMS, NEMS, and Electronic Systems. ASMEDC, 2005. http://dx.doi.org/10.1115/ht2005-72731.

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This paper has provided an innovative aspect in the heat transfer of fuel-cell related studies. A heat/mass coupled modeling approach is presented to predict the transport phenomena inside the porous electrode of a fuel cell. The energy equations based on the local thermal non-equilibrium (LTNE) is derived to resolve the temperature difference between the solid and fluid phases inside the porous electrode. The surface heat transfer is coupled with the species transports via a macroscopic electrochemical model on the reaction boundary. A general criterion for the local thermal non-equilibrium in porous electrodes is first proposed in terms of non-dimensional parameters of engineering importance. Then, the significance of local thermal non-equilibrium in a typical porous electrode is assessed. Furthermore, detailed distributions of the local temperature, local Nusselt number, species concentration, and electric current density inside the porous electrode of fuel cells are presented. Finally, the effect of LTNE parameters on the thermal-fluid behaviors in the porous electrode is investigated.
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Reports on the topic "LTNP"

1

Ali, Zulfiqar, and Valeriy V. Yashchuk. Automated suppression of errors in LTP-II slope measurements with x-ray optics. Part1: Review of LTP errors and methods for the error reduction. Office of Scientific and Technical Information (OSTI), May 2011. http://dx.doi.org/10.2172/1170544.

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Shah, Ayesha, Jan Olek, and Rebecca S. McDaniel. Real Life Experience with Major Pavement Types. Purdue University, 2022. http://dx.doi.org/10.5703/1288284317371.

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Pavement performance is a complex issue which depends on many contributing factors. Examining the performance of real-life pavements across the state determines what the actual service lives are for the pavements. For the purposes of this study, only selected LTPP projects were examined, along with a database containing all the historic repair projects completed in Indiana. Pertinent information present in the Indiana Historic Contracts Database was extracted concerning the types of pavement repair and treatments options commonly employed within the state, the time between repairs, etc. These data were used to determine descriptive statistical parameters and was summarized in graph form. Similarly, data about selected LTPP GPS and SPS sites were downloaded from the online website, LTPP InfoPave and a comparative study between companion sites was performed. These data included study site and pavement-related information, such as construction dates, pavement structure details, maintenance and repair history, and pavement distress surveys. These data were used to draw conclusions about the impact of treatment applications, climatic and geologic factors, traffic volume, and pavement structures on pavement performance. Gaps in knowledge about pavement failure modes, distress data, and effectiveness of treatment applications mentioned in the contracts database file hampered efforts to form a complete picture of the effectiveness of treatment options and their timely (or untimely) application. Similarly, details about pavement mixture design and differentiating factors between companion sites prevented researchers from narrowing down the causes leading to the observed pavement distress.
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Scott, K., and M. Blanchet. Licklider Transmission Protocol (LTP), Compressed Bundle Header Encoding (CBHE), and Bundle Protocol IANA Registries. RFC Editor, February 2014. http://dx.doi.org/10.17487/rfc7116.

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Kruse, H., S. Jero, and S. Ostermann. Datagram Convergence Layers for the Delay- and Disruption-Tolerant Networking (DTN) Bundle Protocol and Licklider Transmission Protocol (LTP). RFC Editor, March 2014. http://dx.doi.org/10.17487/rfc7122.

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Ali, Zulfiqar, and Valeriy V. Yashchuk. Automated suppression of errors in LTP-II slope measurements of x-ray optics. Part 2: Specification for automated rotating/flipping/aligning system. Office of Scientific and Technical Information (OSTI), July 2011. http://dx.doi.org/10.2172/1170543.

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Porat, Ron, Gregory T. McCollum, Amnon Lers, and Charles L. Guy. Identification and characterization of genes involved in the acquisition of chilling tolerance in citrus fruit. United States Department of Agriculture, December 2007. http://dx.doi.org/10.32747/2007.7587727.bard.

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Citrus, like many other tropical and subtropical fruit are sensitive to chilling temperatures. However, application of a pre-storage temperature conditioning (CD) treatment at 16°C for 7 d or of a hot water brushing (HWB) treatment at 60°C for 20 sec remarkably enhances chilling tolerance and reduces the development of chilling injuries (CI) upon storage at 5°C. In the current research, we proposed to identify and characterize grapefruit genes that are induced by CD, and may contribute to the acquisition of fruit chilling tolerance, by two different molecular approaches: cDNA array analysis and PCR cDNA subtraction. In addition, following the recent development and commercialization of the new Affymetrix Citrus Genome Array, we further performed genome-wide transcript profiling analysis following exposure to CD and chilling treatments. To conduct the cDNA array analysis, we constructed cDNA libraries from the peel tissue of CD- and HWB-treated grapefruit, and performed an EST sequencing project including sequencing of 3,456 cDNAs from each library. Based on the obtained sequence information, we chose 70 stress-responsive and chilling-related genes and spotted them on nylon membranes. Following hybridization the constructed cDNA arrays with RNA probes from control and CD-treated fruit and detailed confirmations by RT-PCR analysis, we found that six genes: lipid-transfer protein, metallothionein-like protein, catalase, GTP-binding protein, Lea5, and stress-responsive zinc finger protein, showed higher transcript levels in flavedo of conditioned than in non-conditioned fruit stored at 5 ᵒC. The transcript levels of another four genes: galactinol synthase, ACC oxidase, temperature-induced lipocalin, and chilling-inducible oxygenase, increased only in control untreated fruit but not in chilling-tolerant CD-treated fruit. By PCR cDNA subtraction analysis we identified 17 new chilling-responsive and HWB- and CD-induced genes. Overall, characterization of the expression patterns of these genes as well as of 11 more stress-related genes by RNA gel blot hybridizations revealed that the HWB treatment activated mainly the expression of stress-related genes(HSP19-I, HSP19-II, dehydrin, universal stress protein, EIN2, 1,3;4-β-D-glucanase, and SOD), whereas the CD treatment activated mainly the expression of lipid modification enzymes, including fatty acid disaturase2 (FAD2) and lipid transfer protein (LTP). Genome wide transcriptional profiling analysis using the newly developed Affymetrix Citrus GeneChip® microarray (including 30,171 citrus probe sets) revealed the identification of three different chilling-related regulons: 1,345 probe sets were significantly affected by chilling in both control and CD-treated fruits (chilling-response regulon), 509 probe sets were unique to the CD-treated fruits (chilling tolerance regulon), and 417 probe sets were unique to the chilling-sensitive control fruits (chilling stress regulon). Overall, exposure to chilling led to expression governed arrest of general cellular metabolic activity, including concretive down-regulation of cell wall, pathogen defense, photosynthesis, respiration, and protein, nucleic acid and secondary metabolism. On the other hand, chilling enhanced various adaptation processes, such as changes in the expression levels of transcripts related to membranes, lipid, sterol and carbohydrate metabolism, stress stimuli, hormone biosynthesis, and modifications in DNA binding and transcription factors.
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Sela, Shlomo, and Michael McClelland. Investigation of a new mechanism of desiccation-stress tolerance in Salmonella. United States Department of Agriculture, January 2013. http://dx.doi.org/10.32747/2013.7598155.bard.

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Low-moisture foods (LMF) are increasingly involved in foodborne illness. While bacteria cannot grow in LMF due to the low water content, pathogens such as Salmonella can still survive in dry foods and pose health risks to consumer. We recently found that Salmonella secretes a proteinaceous compound during desiccation, which we identified as OsmY, an osmotic stress response protein of 177 amino acids. To elucidate the role of OsmY in conferring tolerance against desiccation and other stresses in Salmonella entericaserovarTyphimurium (STm), our specific objectives were: (1) Characterize the involvement of OsmY in desiccation tolerance; (2) Perform structure-function analysis of OsmY; (3) Study OsmY expression under various growth- and environmental conditions of relevance to agriculture; (4) Examine the involvement of OsmY in response to other stresses of relevance to agriculture; and (5) Elucidate regulatory pathways involved in controlling osmY expression. We demonstrated that an osmY-mutant strain is impaired in both desiccation tolerance (DT) and in long-term persistence during cold storage (LTP). Genetic complementation and addition of a recombinantOsmY (rOsmY) restored the mutant survival back to that of the wild type (wt). To analyze the function of specific domains we have generated a recombinantOsmY (rOsmY) protein. A dose-response DT study showed that rOsmY has the highest protection at a concentration of 0.5 nM. This effect was protein- specific as a comparable amount of bovine serum albumin, an unrelated protein, had a three-time lower protection level. Further characterization of OsmY revealed that the protein has a surfactant activity and is involved in swarming motility. OsmY was shown to facilitate biofilm formation during dehydration but not during bacterial growth under optimal growth conditions. This finding suggests that expression and secretion of OsmY under stress conditions was potentially associated with facilitating biofilm production. OsmY contains two conserved BON domains. To better understand the role of the BON sites in OsmY-mediated dehydration tolerance, we have generated two additional rOsmY constructs, lacking either BON1 or BON2 sites. BON1-minus (but not BON2) protein has decreased dehydration tolerance compared to intact rOsmY, suggesting that BON1 is required for maximal OsmY-mediated activity. Addition of BON1-peptide at concentration below 0.4 µM did not affect STm survival. Interestingly, a toxic effect of BON1 peptide was observed in concentration as low as 0.4 µM. Higher concentrations resulted in complete abrogation of the rOsmY effect, supporting the notion that BON-mediated interaction is essential for rOsmY activity. We performed extensive analysis of RNA expression of STm undergoing desiccation after exponential and stationary growth, identifying all categories of genes that are differentially expressed during this process. We also performed massively in-parallel screening of all genes in which mutation caused changes in fitness during drying, identifying over 400 such genes, which are now undergoing confirmation. As expected OsmY is one of these genes. In conclusion, this is the first study to identify that OsmY protein secreted during dehydration contributes to desiccation tolerance in Salmonella by facilitating dehydration- mediated biofilm formation. Expression of OsmY also enhances swarming motility, apparently through its surfactant activity. The BON1 domain is required for full OsmY activity, demonstrating a potential intervention to reduce pathogen survival in food processing. Expression and fitness screens have begun to elucidate the processes of desiccation, with the potential to uncover additional specific targets for efforts to mitigate pathogen survival in desiccation.
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