Scientific Resources
Items 37 to 48 of 148 total
- Referencevan Besien K et al. (JUN 2016) Leukemia & lymphoma 0 0 1--10
Cord blood chimerism and relapse after haplo-cord transplantation.
Haplo-cord stem cell transplantation combines the infusion of CD34 selected hematopoietic progenitors from a haplo-identical donor with an umbilical cord blood (UCB) graft from an unrelated donor and allows faster count recovery, with low rates of disease recurrence and chronic graft-versus-host disease (GVHD). But the contribution of the umbilical cord blood graft to long-term transplant outcome remains unclear. We analyzed 39 recipients of haplo-cord transplants with acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS), engrafted and in remission at 2 months. Median age was 66 (18-72) and all had intermediate, high, or very-high risk disease. Less than 20% UCB chimerism in the CD33 lineage was associated with an increased rate of disease recurrence (54% versus 11% p textless 0.0001) and decrease in one year progression-free (20% versus 55%, p = 0.004) and overall survival (30% versus 62%, p = 0.02). Less than 100% UCB chimerism in the CD3 lineage was associated with increase rate of disease recurrence (46% versus 12%, p = 0.007). Persistent haplo-chimerism in the CD3 lineage was associated with an increased rate of disease recurrence (40% versus 15%, p = 0.009) Chimerism did not predict for treatment related mortality. The cumulative incidence of acute GVHD by day 100 was 43%. The cumulative incidence of moderate/severe chronic GVHD was only 5%. Engraftment of the umbilical cord blood grafts provides powerful graft-versus-leukemia (GVL) effects which protect against disease recurrence and is associated with low risk of chronic GVHD. Engraftment of CD34 selected haplo-identical cells can lead to rapid development of circulating T-cells, but when these cells dominate, GVL-effects are limited and rates of disease recurrence are high. View PublicationCatalog #: Product Name: 21000 RoboSep™-S Catalog #: 21000 Product Name: RoboSep™-S ReferenceSzewczyk K et al. (JUN 2016) Human immunology 77 6 449--55Flow cytometry crossmatch reactivity with pronase-treated T cells induced by non-HLA autoantibodies in human immunodeficiency virus-infected patients.
Pronase treatment is used in the flow cytometry crossmatch (FCXM) to prevent nonspecific antibody binding on B cells. However, we have observed unexpected positive results with pronase-treated T cells in human immunodeficiency virus (HIV)-infected patients. In this study, 25 HIV-infected patients without HLA antibodies were tested with pronase-treated and nontreated cells. HIV-positive sera were pretreated with reducing agents and preabsorbed with pronase-treated and nontreated T or B cells before crossmatching. All patients displayed FCXM reactivity with pronase-treated T cells but not with nontreated T cells. None of the patients exhibited FCXM reactivity with pronase-treated and nontreated B cells. These patients displayed FCXM reactivity with pronase-treated CD4+ and CD8+ T cells but not with their nontreated counterparts. Preabsorption with pronase-treated T cells reduced the T cell FCXM reactivity. Preabsorption with pronase-treated B cells or nontreated T and B cells did not have any effect on the T cell FCXM reactivity. Pretreatment with reducing agents did not affect the T cell FCXM reactivity. 15 of 21 HIV-infected kidney allograft recipients with pronase-treated T cell FCXM reactivity display long-term graft survival (1193±631days). These data indicate that HIV-infected patients have nondeleterious autoantibodies recognizing cryptic epitopes exposed by pronase on T cells. View PublicationCatalog #: Product Name: 17952 EasySep™ Human CD4+ T Cell Isolation Kit 17953 EasySep™ Human CD8+ T Cell Isolation Kit 21000 RoboSep™-S Catalog #: 17952 Product Name: EasySep™ Human CD4+ T Cell Isolation Kit Catalog #: 17953 Product Name: EasySep™ Human CD8+ T Cell Isolation Kit Catalog #: 21000 Product Name: RoboSep™-S ReferenceY. Kuwano et al. (MAY 2016) Journal of Immunology 196 9 3828--33G$\alpha$i2 and G$\alpha$i3 Differentially Regulate Arrest from Flow and Chemotaxis in Mouse Neutrophils.
Leukocyte recruitment to inflammation sites progresses in a multistep cascade. Chemokines regulate multiple steps of the cascade, including arrest, transmigration, and chemotaxis. The most important chemokine receptor in mouse neutrophils is CXCR2, which couples through G$\alpha$i2- and G$\alpha$i3-containing heterotrimeric G proteins. Neutrophils arrest in response to CXCR2 stimulation. This is defective in G$\alpha$i2-deficient neutrophils. In this study, we show that G$\alpha$i3-deficient neutrophils showed reduced transmigration but normal arrest in mice. We also tested G$\alpha$i2- or G$\alpha$i3-deficient neutrophils in a CXCL1 gradient generated by a microfluidic device. G$\alpha$i3-, but not G$\alpha$i2-, deficient neutrophils showed significantly reduced migration and directionality. This was confirmed in a model of sterile inflammation in vivo. G$\alpha$i2-, but not G$\alpha$i3-, deficient neutrophils showed decreased Ca(2+) flux in response to CXCR2 stimulation. Conversely, G$\alpha$i3-, but not G$\alpha$i2-, deficient neutrophils exhibited reduced AKT phosphorylation upon CXCR2 stimulation. We conclude that G$\alpha$i2 controls arrest and G$\alpha$i3 controls transmigration and chemotaxis in response to chemokine stimulation of neutrophils. View PublicationCatalog #: Product Name: 21000 RoboSep™-S 19762 EasySep™ Mouse Neutrophil Enrichment Kit Catalog #: 21000 Product Name: RoboSep™-S Catalog #: 19762 Product Name: EasySep™ Mouse Neutrophil Enrichment Kit ReferenceKarpinski J et al. (APR 2016) Nature Biotechnology 34 4 401--9Directed evolution of a recombinase that excises the provirus of most HIV-1 primary isolates with high specificity.
Current combination antiretroviral therapies (cART) efficiently suppress HIV-1 reproduction in humans, but the virus persists as integrated proviral reservoirs in small numbers of cells. To generate an antiviral agent capable of eradicating the provirus from infected cells, we employed 145 cycles of substrate-linked directed evolution to evolve a recombinase (Brec1) that site-specifically recognizes a 34-bp sequence present in the long terminal repeats (LTRs) of the majority of the clinically relevant HIV-1 strains and subtypes. Brec1 efficiently, precisely and safely removes the integrated provirus from infected cells and is efficacious on clinical HIV-1 isolates in vitro and in vivo, including in mice humanized with patient-derived cells. Our data suggest that Brec1 has potential for clinical application as a curative HIV-1 therapy. View PublicationCatalog #: Product Name: 02697 StemSpan™ CC110 17896 EasySep™ Human Cord Blood CD34 Positive Selection Kit II 17952 EasySep™ Human CD4+ T Cell Isolation Kit 21000 RoboSep™-S 04435 MethoCult™ H4435 Enriched Catalog #: 02697 Product Name: StemSpan™ CC110 Catalog #: 17896 Product Name: EasySep™ Human Cord Blood CD34 Positive Selection Kit II Catalog #: 17952 Product Name: EasySep™ Human CD4+ T Cell Isolation Kit Catalog #: 21000 Product Name: RoboSep™-S Catalog #: 04435 Product Name: MethoCult™ H4435 Enriched ReferenceHaase D et al. ( ) Journal of immunotherapy (Hagerstown, Md. : 1997) 38 6 250--8Large-scale Isolation of Highly Pure Untouched" Regulatory T Cells in a GMP Environment for Adoptive Cell Therapy."
Adoptive cell therapy is an emerging treatment strategy for a number of serious diseases. Regulatory T (Treg) cells represent 1 cell type of particular interest for therapy of inflammatory conditions, as they are responsible for controlling unwanted immune responses. Initial clinical trials of adoptive transfer of Treg cells in patients with graft-versus-host disease were shown to be safe. However, obtaining sufficient numbers of highly pure and functional Treg cells with minimal contamination remains a challenge. We developed a novel approach to isolate untouched" human Treg cells from healthy donors on the basis of negative selection using the surface markers CD49d and CD127. This procedure� View PublicationCatalog #: Product Name: 21000 RoboSep™-S Catalog #: 21000 Product Name: RoboSep™-S ReferenceMaricato JT et al. ( 2015) PloS One 10 4 e0119234Epigenetic Modulations in Activated Cells Early after HIV-1 Infection and Their Possible Functional Consequences
Epigenetic modifications refer to a number of biological processes which alter the structure of chromatin and its transcriptional activity such as DNA methylation and histone post-translational processing. Studies have tried to elucidate how the viral genome and its products are affected by epigenetic modifications imposed by cell machinery and how it affects the ability of the virus to either, replicate and produce a viable progeny or be driven to latency. The purpose of this study was to evaluate epigenetic modifications in PBMCs and CD4+ cells after HIV-1 infection analyzing three approaches: (i) global DNA- methylation; (ii) qPCR array and (iii) western blot. HIV-1 infection led to methylation increases in the cellular DNA regardless the activation status of PBMCs. The analysis of H3K9me3 and H3K27me3 suggested a trend towards transcriptional repression in activated cells after HIV-1 infection. Using a qPCR array, we detected genes related to epigenetic processes highly modulated in activated HIV-1 infected cells. SETDB2 and RSK2 transcripts showed highest up-regulation levels. SETDB2 signaling is related to transcriptional silencing while RSK2 is related to either silencing or activation of gene expression depending on the signaling pathway triggered down-stream. In addition, activated cells infected by HIV-1 showed lower CD69 expression and a decrease of IL-2, IFN-γ and metabolism-related factors transcripts indicating a possible functional consequence towards global transcriptional repression found in HIV-1 infected cells. Conversely, based on epigenetic markers studied here, non-stimulated cells infected by HIV-1, showed signs of global transcriptional activation. Our results suggest that HIV-1 infection exerts epigenetic modulations in activated cells that may lead these cells to transcriptional repression with important functional consequences. Moreover, non-stimulated cells seem to increase gene transcription after HIV-1 infection. Based on these observations, it is possible to speculate that the outcome of viral infections may be influenced by the cellular activation status at the moment of infection. View PublicationCatalog #: Product Name: 21000 RoboSep™-S Catalog #: 21000 Product Name: RoboSep™-S ReferenceChevalier MF et al. ( 2015) The Journal of Infectious Diseases 211 5 769--779Phenotype Alterations in Regulatory T-Cell Subsets in Primary HIV Infection and Identification of Tr1-like Cells as the Main Interleukin 10-Producing CD4+ T Cells
BACKGROUND: Conventional regulatory T cells (Tregs) can suppress human immunodeficiency virus type 1 (HIV-1)-specific immune responses but cannot control immune activation in primary HIV infection. Here, we characterized Treg subsets, using recently defined phenotypic delineation, and analyzed the relative contribution of cell subsets to the production of immunosuppressive cytokines in primary HIV infection. METHODS: In a longitudinal prospective study, ex vivo phenotyping of fresh peripheral blood mononuclear cells from patients with primary HIV infection was performed at baseline and month 6 of follow-up to characterize Treg subsets, immune activation, and cytokine production in isolated CD4(+) T cells. RESULTS: The frequency of CD4(+)CD25(+)CD127(low) Tregs and the distribution between the naive, memory, and activated/memory Treg subsets was similar in patients and healthy donors. However, Tregs from patients with primary HIV infection showed peculiar phenotypic profiles, such as elevated FoxP3, ICOS, and CTLA-4 expression, with CTLA-4 expression strikingly increased in all Treg subsets both at baseline and month 6 of follow-up. The great majority of interleukin 10 (IL-10)-producing CD4(+) T cells were FoxP3(neg) (ie, Tr1-like cells). In contrast to conventional Tregs, Tr1-like cells were inversely correlated with immune activation and not associated with lower effector T-cell responses. CONCLUSION: FoxP3(neg) Tr1-like cells-major contributors to IL-10 production-may have a beneficial role by controlling immune activation in early HIV infection. View PublicationCatalog #: Product Name: 15022 RosetteSep™ Human CD4+ T Cell Enrichment Cocktail 21000 RoboSep™-S Catalog #: 15022 Product Name: RosetteSep™ Human CD4+ T Cell Enrichment Cocktail Catalog #: 21000 Product Name: RoboSep™-S ReferenceBae J et al. (JAN 2015) Leukemia 29 1 218--29A multiepitope of XBP1, CD138 and CS1 peptides induces myeloma-specific cytotoxic T lymphocytes in T cells of smoldering myeloma patients.
We evaluated a cocktail of HLA-A2-specific peptides including heteroclitic XBP1 US184-192 (YISPWILAV), heteroclitic XBP1 SP367-375 (YLFPQLISV), native CD138260-268 (GLVGLIFAV) and native CS1239-247 (SLFVLGLFL), for their ability to elicit multipeptide-specific cytotoxic T lymphocytes (MP-CTLs) using T cells from smoldering multiple myeloma (SMM) patients. Our results demonstrate that MP-CTLs generated from SMM patients' T cells show effective anti-MM responses including CD137 (4-1BB) upregulation, CTL proliferation, interferon-γ production and degranulation (CD107a) in an HLA-A2-restricted and peptide-specific manner. Phenotypically, we observed increased total CD3(+)CD8(+) T cells (textgreater80%) and cellular activation (CD69(+)) within the memory SMM MP-CTL (CD45RO(+)/CD3(+)CD8(+)) subset after repeated multipeptide stimulation. Importantly, SMM patients could be categorized into distinct groups by their level of MP-CTL expansion and antitumor activity. In high responders, the effector memory (CCR7(-)CD45RO(+)/CD3(+)CD8(+)) T-cell subset was enriched, whereas the remaining responders' CTL contained a higher frequency of the terminal effector (CCR7(-)CD45RO(-)/CD3(+)CD8(+)) subset. These results suggest that this multipeptide cocktail has the potential to induce effective and durable memory MP-CTL in SMM patients. Therefore, our findings provide the rationale for clinical evaluation of a therapeutic vaccine to prevent or delay progression of SMM to active disease. View PublicationCatalog #: Product Name: 19051 EasySep™ Human T Cell Enrichment Kit 21000 RoboSep™-S Catalog #: 19051 Product Name: EasySep™ Human T Cell Enrichment Kit Catalog #: 21000 Product Name: RoboSep™-S ReferenceTyznik AJ et al. ( 2014) The Journal of Immunology 192 8 3676--85Distinct requirements for activation of NKT and NK cells during viral infection
NK cells are key regulators of innate defense against mouse CMV (MCMV). Like NK cells, NKT cells also produce high levels of IFN-γ rapidly after MCMV infection. However, whether similar mechanisms govern activation of these two cell types, as well as the significance of NKT cells for host resistance, remain unknown. In this article, we show that, although both NKT and NK cells are activated via cytokines, their particular cytokine requirements differ significantly in vitro and in vivo. IL-12 is required for NKT cell activation in vitro but is not sufficient, whereas NK cells have the capacity to be activated more promiscuously in response to individual cytokines from innate cells. In line with these results, GM-CSF-derived dendritic cells activated only NK cells upon MCMV infection, consistent with their virtual lack of IL-12 production, whereas Flt3 ligand-derived dendritic cells produced IL-12 and activated both NK and NKT cells. In vivo, NKT cell activation was abolished in IL-12(-/-) mice infected with MCMV, whereas NK cells were still activated. In turn, splenic NK cell activation was more IL-18 dependent. The differential requirements for IL-12 and IL-18 correlated with the levels of cytokine receptor expression by NK and NKT cells. Finally, mice lacking NKT cells showed reduced control of MCMV, and depleting NK cells further enhanced viral replication. Taken together, our results show that NKT and NK cells have differing requirements for cytokine-mediated activation, and both can contribute nonredundantly to MCMV defense, revealing that these two innate lymphocyte subsets function together to fine-tune antiviral responses. View PublicationCatalog #: Product Name: 21000 RoboSep™-S Catalog #: 21000 Product Name: RoboSep™-S ReferenceHanson V et al. (OCT 2013) Tissue antigens 82 4 269--75Assessment of the purity of isolated cell populations for lineage-specific chimerism monitoring post haematopoietic stem cell transplantation.
Following haematopoietic stem cell transplantation, monitoring the proportion of donor and recipient haematopoiesis in the patient (chimerism) is an influential tool in directing further treatment choices. Short tandem repeat (STR) analysis is a method of chimerism monitoring using DNA isolated from peripheral blood, bone marrow or specific isolated cell lineages such as CD3+ T cells. For lineage-specific STR analysis on cell populations isolated from peripheral blood, a qualitative estimation of the purity of each isolated population is essential for the correct interpretation of the test data. We describe a rapid, inexpensive method for the determination of purity using a simple flow cytometry method. The method described for assessing the purity of sorted CD3+ cells can be applied to any cell population isolated using the same technology. Data obtained were comparable to results from a commercial polymerase chain reaction (PCR)-based method for the assessment of purity (Non-T Genomic Detection Kit, Accumol, Calgary, AB, Canada) (P = 0.59). Of the 303 samples tested by flow cytometry, 290 (95.7%) exceeded 90% purity, and 215 (70.95%) were over 99% pure. There were some outlying samples, showing diversity between samples and the unpredictability of purity of isolated cell populations. This flow cytometry method can be easily assimilated into routine testing protocols, allowing purity assessment in multiple-sorted cell populations for lineage-specific chimerism monitoring using a single secondary antibody and giving results comparable to a PCR-based method. As purity of isolated cell lineages is affected by time after venepuncture and storage temperature, assessment of each sample is recommended to give a reliable indication of sample quality and confidence in the interpretation of the results. View PublicationCatalog #: Product Name: 21000 RoboSep™-S Catalog #: 21000 Product Name: RoboSep™-S ReferenceSá et al. (JUL 2011) Blood 118 4 955--64Restriction of HIV-1 replication in macrophages and CD4+ T cells from HIV controllers.
How HIV controllers (HICs) maintain undetectable viremia without therapy is unknown. The strong CD8(+) T-cell HIV suppressive capacity found in many, but not all, HICs may contribute to long-lasting viral control. However, other earlier defense mechanisms may be involved. Here, we examined intrinsic HIC cell resistance to HIV-1 infection. After in vitro challenge, monocyte-derived macrophages and anti-CD3-activated CD4(+) T cells from HICs showed low HIV-1 susceptibility. CD4 T-cell resistance was independent of HIV-1 coreceptors and affected also SIVmac infection. CD4(+) T cells from HICs expressed ex vivo higher levels of p21(Waf1/Cip1), which has been involved in the control of HIV-1 replication, than cells from control subjects. However, HIV restriction in anti-CD3-activated CD4(+) T cells and macrophages was not associated with p21 expression. Restriction inhibited accumulation of reverse transcripts, leading to reduction of HIV-1 integrated proviruses. The block could be overcome by high viral inocula, suggesting the action of a saturable mechanism. Importantly, cell-associated HIV-1 DNA load was extremely low in HICs and correlated with CD4(+) T-cell permissiveness to infection. These results point to a contribution of intrinsic cell resistance to the control of infection and the containment of viral reservoir in HICs. View PublicationCatalog #: Product Name: 21000 RoboSep™-S Catalog #: 21000 Product Name: RoboSep™-S ReferenceWang E et al. (FEB 2011) American journal of clinical pathology 135 2 291--303Pseudo-Pelger-Huët anomaly induced by medications: a clinicopathologic study in comparison with myelodysplastic syndrome-related pseudo-Pelger-Huët anomaly.
Pseudo-Pelger-Huët anomaly (PPHA) has been documented in association with transplant medications and other drugs. This iatrogenic neutrophilic dysplasia is reversible with cessation or adjustment of medications but is frequently confused with myelodysplastic syndrome (MDS) based on the conventional concept that PPHA is a marker for dysplasia. We investigated the clinicopathologic features in iatrogenic PPHA and compared them with MDS-related PPHA. The 13 cases studied included 5 bone marrow/stem cell transplantations, 3 solid organ transplantations, 1 autoimmune disease, 3 chronic lymphocytic leukemias, and 1 breast carcinoma. For 12 cases, there was follow-up evaluation, and all demonstrated at least transient normalization of neutrophilic segmentation. All 9 cases of MDS demonstrated at least 2 of the following pathologic abnormalities on bone marrow biopsy: hypercellularity (8/9), morphologic dysplasia (8/9), clonal cytogenetic abnormality (7/9), and increased blasts (3/9), whereas these abnormalities were typically absent in iatrogenic PPHA. Iatrogenic PPHA displayed a higher proportion of circulating PPHA cells than in MDS (mean, 47.4%; SD, 31.6% vs mean, 12.3%; SD, 9.8; P textless .01). A diagnostic algorithm is proposed in which isolated PPHA is indicative of transient or benign PPHA unless proven otherwise. View PublicationCatalog #: Product Name: 21000 RoboSep™-S Catalog #: 21000 Product Name: RoboSep™-S Items 37 to 48 of 148 total
Shop ByFilter ResultsFilters:- Brand RoboSep Remove This Item
- Clear All
- Resource Type
- Brochure 13 items
- Interview 1 item
- Protocol 1 item
- Reference 64 items
- Scientific Poster 29 items
- Tech Tip 10 items
- Technical Bulletin 4 items
- Technical Manual 2 items
- Video 10 items
- Wallchart 8 items
- Webinar 6 items
- Area of Interest
- Cancer 17 items
- Cell Therapy Research 6 items
- Chimerism 11 items
- Disease Modeling 1 item
- Drug Discovery and Toxicity Testing 7 items
- Epithelial Cell Biology 1 item
- HIV 7 items
- HLA 20 items
- Immunology 94 items
- Infectious Diseases 5 items
- Neuroscience 1 item
- Organoids 1 item
- Respiratory Research 1 item
- Stem Cell Biology 6 items
- Transplantation Research 4 items
- Brand
- RoboSep 148 items
- ALDECOUNT 14 items
- ALDEFLUOR 215 items
- AggreWell 85 items
- ArciTect 37 items
- BloodStor 1 item
- BrainPhys 75 items
- CellAdhere 2 items
- ClonaCell 108 items
- CloneR 7 items
- CryoStor 76 items
- DermaCult 1 item
- EC-Cult 2 items
- ELISA 4 items
- ES-Cult 95 items
- EasyPick 2 items
- EasySep 974 items
- EpiCult 24 items
- ErythroClear 3 items
- HemaTox 6 items
- HepatiCult 20 items
- HetaSep 1 item
- Hypothermosol 1 item
- ImmunoCult 49 items
- IntestiCult 189 items
- Lymphoprep 34 items
- MammoCult 31 items
- Matrigel 1 item
- MegaCult 41 items
- MesenCult 171 items
- MethoCult 554 items
- MyeloCult 81 items
- MyoCult 7 items
- NaïveCult 1 item
- NeuroCult 403 items
- NeuroFluor 4 items
- PancreaCult 9 items
- PneumaCult 113 items
- ProstaCult 4 items
- RSeT 16 items
- ReLeSR 11 items
- RosetteSep 324 items
- STEMdiff 243 items
- STEMgrid 2 items
- STEMscript 1 item
- STEMtaq 1 item
- STEMvision 32 items
- SepMate 71 items
- SmartDish 10 items
- StemSep 14 items
- StemSpan 348 items
- TeSR 1734 items
- ThawSTAR 4 items
- mFreSR 37 items
- Cell Type
- Airway Cells 1 item
- B Cells 27 items
- Cancer Cells and Cell Lines 1 item
- Dendritic Cells 14 items
- Epithelial Cells 1 item
- Granulocytes and Subsets 15 items
- Hematopoietic Stem and Progenitor Cells 12 items
- Innate Lymphoid Cells 4 items
- Intestinal Cells 1 item
- Leukocytes 3 items
- Leukopaks 3 items
- Lymphocytes 17 items
- Macrophages 7 items
- Mammary Cells 2 items
- Mesenchymal Stem and Progenitor Cells 1 item
- Mesenchymal Stromal Cells 1 item
- Monocytes 19 items
- Mononuclear Cells 11 items
- Myeloid Cells 13 items
- Myeloma 1 item
- NK Cells 15 items
- Neural Stem and Progenitor Cells 1 item
- Pancreatic Cells 1 item
- Plasma 2 items
- Platelets 1 item
- Pluripotent Stem Cells 1 item
- Prostate Cells 1 item
- T Cells 46 items
- T Cells, CD4+ 21 items
- T Cells, CD8+ 18 items
- T Cells, Other Subsets 7 items
- T Cells, Regulatory 13 items
- Whole 1 item
Loading...Contact STEMCELL Technologies
StemCell Technologies Inc. and affiliates ("STEMCELL Technologies") does not share your email address with third parties. StemCell Technologies Inc. will use your email address to confirm your identity and send you newsletters, transaction-related emails, promotional and customer service emails in accordance with our privacy policy. You can change your email preferences at any time.
Copyright © 2022 by STEMCELL Technologies Inc. All rights reserved.