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Journal articles on the topic 'LLT1'

Author: Grafiati

Published: 4 June 2021

Last updated: 14 February 2022

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1

Llibre, Alba, Lucy Garner, Amy Partridge, Gordon J. Freeman, Paul Klenerman, and Chris B. Willberg. "Expression of lectin-like transcript-1 in human tissues." F1000Research 5 (December 29, 2016): 2929. http://dx.doi.org/10.12688/f1000research.10009.1.

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Background: Receptor-ligand pairs of C-type lectin-like proteins have been shown to play an important role in cross talk between lymphocytes, as well as in immune responses within concrete tissues and structures, such as the skin or the germinal centres. The CD161-Lectin-like Transcript 1 (LLT1) pair has gained particular attention in recent years, yet a detailed analysis of LLT1 distribution in human tissue is lacking. One reason for this is the limited availability and poor characterisation of anti-LLT1 antibodies. Methods: We assessed the staining capabilities of a novel anti-LLT1 antibody clone (2H7), both by immunohistochemistry and flow cytometry, showing its efficiency at LLT1 recognition in both settings. We then analysed LLT1 expression in a wide variety of human tissues. Results: We found LLT1 expression in circulating B cells and monocytes, but not in lung and liver-resident macrophages. We found strikingly high LLT1 expression in immune-privileged sites, such as the brain, placenta and testes, and confirmed the ability of LLT1 to inhibit NK cell function. Conclusions: Overall, this study contributes to the development of efficient tools for the study of LLT1. Moreover, its expression in different healthy human tissues and, particularly, in immune-privileged sites, establishes LLT1 as a good candidate as a regulator of immune responses.

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Ghosh, Maloy, Kavitha Iyer Rodrigues, Sunit Maity, Sanghamitra Bhattacharjee, Yogendra Manjunath, Subhra Prakash Chakrabarty, Ashvini Kumar Dubey, Anurag Tiwari, Sathyabalan Murugesan, and Vivek Halan. "Novel monoclonal antibody therapeutics for metastatic castration resistant prostate cancer." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): e14222-e14222. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e14222.

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e14222 Background: Therapeutic potential of innate immunity comprising Natural killer cell based targets are beginning to unravel the complexity of immune responses. NK cells recognize and induce cytotoxicity of wide range of target cells, such as, tumor cells without prior antigen sensitization. In this study, we have studied Lectin-like transcript 1 (LLT1), a member of the C-type lectin super family, is expressed on target cells and various immune cells. LLT1 isoform 1, is known to interact with CD161, a critical receptor on NK cells. CD161 is expressed on most of human NK cells, NK-T cells, γδ T cells and so on. Tumors exploit the CD161- LLT1 interaction to evade host defense mechanism (“DO NOT KILL” signal); indicating LLT1 as an attractive immunotherapeutic strategy. Methods: Prostate cancer cell lines and other tumor cell lines were used to evaluate novel anti LLT1 antibodies for therapeutic potential - IFNγ production assays and tumor cell death assays were carried out. In vivo efficacy of these antibodies were established using PC3 xenograft in humanized mouse model (HuNOG-EXL). Results: Human androgen independent prostate cancer cell line, PC3 was studied for LLT1 expression and interactions with immune cells, to understand role of LLT1 in metastatic castration resistant prostate cancer (mCRPC). Overexpression of LLT1 on tumor cells was influenced by cytokines and various TLRs. Inhibition of CD161-LLT1 interaction with novel anti LLT1 antibodies leads to IFNγ production and consequent NK cell mediated cytotoxicity – hall mark of anti-tumor responses. Disruption of LLT1 - CD161 innate immunity axis with anti LLT1 antibody releases the break on NK cell cytotoxicity and hence, established a new therapeutic option. PC3 xenograft on HuNOG mouse revealed in vivo efficacy of LLT1 antibody. Significant tumor growth reduction was observed with specific anti LLT1 antibodies alone and in combination with check point antibodies. Thus, synergistic tumor growth reduction was established by combinatorial application of anti LLT1 antibody and PD1/PDL1 axis inhibitors. Conclusions: PC3 xenograft study and other results point to therapeutic opportunities in metastatic castration resistant prostate cancer, a disease condition which needs improved patient outcomes. The ligation of CD161/LLT1 will serve as a new immuno-oncology pair regulating innate and adaptive immune responses; novel human antibodies against LLT1 described here will bring therapeutic benefit to patients in need.

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3

Sanchez-Canteli, Mario, Francisco Hermida-Prado, Christian Sordo-Bahamonde, Irene Montoro-Jiménez, Esperanza Pozo-Agundo, Eva Allonca, Aitana Vallina-Álvarez, et al. "Lectin-Like Transcript 1 (LLT1) Checkpoint: A Novel Independent Prognostic Factor in HPV-Negative Oropharyngeal Squamous Cell Carcinoma." Biomedicines 8, no. 12 (November 25, 2020): 535. http://dx.doi.org/10.3390/biomedicines8120535.

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Lectin-like transcript 1 (LLT1) expression by tumor cells contributes to immune evasion, thereby emerging as a natural killer (NK) cell-mediated immunotherapeutic target. This study is the first to investigate LLT1 expression (encoded by CLEC2D gene) in head and neck cancers to ascertain its impact on patient prognosis. LLT1 expression was analyzed by immunohistochemistry in a homogeneous cohort of human papillomavirus (HPV)-negative oropharyngeal squamous cell carcinomas (OPSCC), and correlated with clinical data. Results were further validated using transcriptomic data from the TCGA database. Tumoral LLT1 expression was detected in 190/221 (86%) OPSCC specimens, whereas normal pharyngeal epithelium was negative. Patients harboring LLT1-positive tumors showed significantly lower disease-specific (DSS) and overall survival (OS) (p = 0.049 and p = 0.036, respectively, log-rank test). High density of LLT1-positive tumor-infiltrating lymphocytes (TIL) was also frequently detected in 160 (73%) OPSCC samples, and significantly associated with better DSS and OS (p < 0.001 and p = 0.007, respectively). Multivariate Cox analysis further revealed that tumoral LLT1 expression and infiltration of LLT1-positive TIL were independent prognostic factors for DSS and OS. CLEC2D mRNA levels are also significantly increased in primary tumors compared to normal tissue. Strikingly, the prognostic impact of CLEC2D mRNA levels varied depending on HPV status in OPSCC, and among distinct cancer types. CLEC2D expression was significantly correlated with NK cell infiltration using the MCP-counter model. These findings uncover LLT1/CLEC2D as an independent prognostic factor in HPV-negative OPSCC, and a potential novel target for immunotherapy.

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4

Skálová, Tereza, Jan Bláha, Karl Harlos, Jarmila Dušková, Tomáš Koval', Jan Stránský, Jindřich Hašek, Ondřej Vaněk, and Jan Dohnálek. "Four crystal structures of human LLT1, a ligand of human NKR-P1, in varied glycosylation and oligomerization states." Acta Crystallographica Section D Biological Crystallography 71, no. 3 (February 26, 2015): 578–91. http://dx.doi.org/10.1107/s1399004714027928.

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Human LLT1 is a C-type lectin-like ligand of NKR-P1 (CD161, geneKLRB1), a C-type lectin-like receptor of natural killer cells. Using X-ray diffraction, the first experimental structures of human LLT1 were determined. Four structures of LLT1 under various conditions were determined: monomeric, dimeric deglycosylated after the firstN-acetylglucosamine unit in two forms and hexameric with homogeneous GlcNAc2Man5glycosylation. The dimeric form follows the classical dimerization mode of human CD69. The monomeric form keeps the same fold with the exception of the position of an outer part of the long loop region. The hexamer of glycosylated LLT1 consists of three classical dimers. The hexameric packing may indicate a possible mode of interaction of C-type lectin-like proteins in the glycosylated form.

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5

Buller, Casey W., Porunelloor A. Mathew, and Stephen O. Mathew. "Roles of NK Cell Receptors 2B4 (CD244), CS1 (CD319), and LLT1 (CLEC2D) in Cancer." Cancers 12, no. 7 (July 1, 2020): 1755. http://dx.doi.org/10.3390/cancers12071755.

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Natural killer (NK) cells play a pivotal role in the immune system, especially in the recognition and clearance of cancer cells and infected cells. Their effector function is controlled by a delicate balance between the activating and inhibitory signals. We have identified 2B4 (CD244, SLAMF4) and CS1 (CD319, SLAMF7) as NK cell receptors regulating NK cell cytotoxicity. Lectin-like transcript 1 (LLT1), a member of the C-type lectin-like domain family 2 (CLEC2D), induced IFN-γ production but did not directly regulate cytolytic activity. Interestingly, LLT1 expressed on other cells acts as a ligand for an NK cell inhibitory receptor NKRP1A (CD161) and inhibits NK cytolytic function. Extensive research has been done on novel therapies that target these receptors to increase the effector function of NK cells. The 2B4 receptor is involved in the rejection of melanoma cells in mice. Empliciti, an FDA-approved monoclonal antibody, explicitly targets the CS1 receptor and enhances the NK cell cytotoxicity against multiple myeloma cells. Our studies revealed that LLT1 is expressed on prostate cancer and triple-negative breast cancer cells and allows them to evade NK-cell-mediated killing. In this review, we describe NK cell receptors 2B4, CS1, and LLT1 and their potential in targeting cancer cells for NK-cell-mediated immunotherapy. New cancer immunotherapies like chimeric antigen receptor T (CAR-T) and NK (CAR-NK) cells are showing great promise in the treatment of cancer, and CAR cells specific to these receptors would be an attractive therapeutic option.

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6

Mathew, Stephen O., Pankaj Chaudhary, Sheila B. Powers, Jamboor K. Vishwanatha, and Porunelloor A. Mathew. "Overexpression of LLT1 (OCIL, CLEC2D) on prostate cancer cells inhibits NK cell-mediated killing through LLT1-NKRP1A (CD161) interaction." Oncotarget 7, no. 42 (September 8, 2016): 68650–61. http://dx.doi.org/10.18632/oncotarget.11896.

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7

Mahjoub, Nada, Sophie Dhorne-Pollet, Walter Fuchs, Marie-Laure Endale Ahanda, Elke Lange, Barbara Klupp, Anoop Arya, et al. "A 2.5-Kilobase Deletion Containing a Cluster of Nine MicroRNAs in the Latency-Associated-Transcript Locus of the Pseudorabies Virus Affects the Host Response of Porcine Trigeminal Ganglia during Established Latency." Journal of Virology 89, no. 1 (October 15, 2014): 428–42. http://dx.doi.org/10.1128/jvi.02181-14.

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ABSTRACTThe alphaherpesvirus pseudorabies virus (PrV) establishes latency primarily in neurons of trigeminal ganglia when only the transcription of the latency-associated transcript (LAT) locus is detected. Eleven microRNAs (miRNAs) cluster within the LAT, suggesting a role in establishment and/or maintenance of latency. We generated a mutant (M) PrV deleted of nine miRNA genes which displayed properties that were almost identical to those of the parental PrV wild type (WT) during propagationin vitro. Fifteen pigs were experimentally infected with either WT or M virus or were mock infected. Similar levels of virus excretion and host antibody response were observed in all infected animals. At 62 days postinfection, trigeminal ganglia were excised and profiled by deep sequencing and quantitative RT-PCR. Latency was established in all infected animals without evidence of viral reactivation, demonstrating that miRNAs are not essential for this process. Lower levels of the large latency transcript (LLT) were found in ganglia infected by M PrV than in those infected by WT PrV. All PrV miRNAs were expressed, with highest expression observed for prv-miR-LLT1, prv-miR-LLT2 (in WT ganglia), and prv-miR-LLT10 (in both WT and M ganglia). No evidence of differentially expressed porcine miRNAs was found. Fifty-four porcine genes were differentially expressed between WT, M, and control ganglia. Both viruses triggered a strong host immune response, but in M ganglia gene upregulation was prevalent. Pathway analyses indicated that several biofunctions, including those related to cell-mediated immune response and the migration of dendritic cells, were impaired in M ganglia. These findings are consistent with a function of the LAT locus in the modulation of host response for maintaining a latent state.IMPORTANCEThis study provides a thorough reference on the establishment of latency by PrV in its natural host, the pig. Our results corroborate the evidence obtained from the study of several LAT mutants of other alphaherpesviruses encoding miRNAs from their LAT regions. Neither PrV miRNA expression nor high LLT expression levels are essential to achieve latency in trigeminal ganglia. Once latency is established by PrV, the only remarkable differences are found in the pattern of host response. This indicates that, as in herpes simplex virus, LAT functions as an immune evasion locus.

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8

Kamishikiryo, Jun, Hideo Fukuhara, Yuki Okabe, Kimiko Kuroki, and Katsumi Maenaka. "Molecular Basis for LLT1 Protein Recognition by Human CD161 Protein (NKRP1A/KLRB1)." Journal of Biological Chemistry 286, no. 27 (May 13, 2011): 23823–30. http://dx.doi.org/10.1074/jbc.m110.214254.

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Human Th17 cells express high levels of CD161, a member of the killer cell lectin-like receptor (KLR) family (also referred to as NK receptor-P1A (NKRP1A) or KLRB1), as a representative marker. CD161 is also expressed on natural killer (NK) cells and NKT cells. Lectin-like transcript 1 (LLT1), another KLR family member, was recently identified as a ligand for CD161. This interaction may play pivotal roles in the immunomodulatory functions of Th17 cells as well as those of NK and NKT cells. However, the molecular basis for the interaction is poorly understood. Here we show that the extracellular domain of CD161 bound directly to LLT1 with a Kd of 48 μm and with the fast kinetics typical of cell-cell recognition receptors. Mutagenesis revealed that the similar membrane-distal β-sheet and loop regions of both CD161 and LLT1 were utilized for the binding, and notably, these regions correspond to the ligand-binding sites for major histocompatibility complex (MHC)-recognizing KLRs. Furthermore, we found a pair of detrimental mutations for both molecules that restored the binding. These results reveal a new template model for the recognition mode between the KLR family members and provide insights into the molecular mechanism underlying Th17/NK/NKT-mediated immune responses.

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9

Bialoszewska, Agata, and Jacek Malejczyk. "Biological and Clinical Significance of Human NKRP1A/LLT1 Receptor/Ligand Interactions." Critical Reviews in Immunology 38, no. 6 (2018): 479–89. http://dx.doi.org/10.1615/critrevimmunol.2019029559.

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10

Mathew, P. "The LLT1 receptor induces IFN-γ production by human natural killer cells." Molecular Immunology 40, no. 16 (March 2004): 1157–63. http://dx.doi.org/10.1016/j.molimm.2003.11.024.

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11

Shunsuke, Kita, Matsubara Haruki, Kamishikiryo Jun, Okabe Yuki, Fukuhara Hideo, Kuroki Kimiko, and Maenaka Katsumi. "1P005 Structure analysis of lectin-like transcript 1 (LLT1) and model building of LLT1-CD161 complex(Protein: Structure,Poster,The 52th Annual Meeting of the Biophysical Society of Japan(BSJ2014))." Seibutsu Butsuri 54, supplement1-2 (2014): S141. http://dx.doi.org/10.2142/biophys.54.s141_5.

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12

Purbhoo, M. A., N. Kumar, and S. Ashraf. "805 LLT1 ENGAGES CD161 AT THE IMMUNOLOGICAL SYNAPSE BETWEEN T CELLS AND HEPATOCYTES." Journal of Hepatology 56 (April 2012): S315. http://dx.doi.org/10.1016/s0168-8278(12)60817-4.

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13

Skálová, Tereza, Jan Bláha, Karl Harlos, Jarmila Dušková, Tomáš Koval', Jan Stránský, Jindřich Hašek, Ondřej Vaněk, and Jan Dohnálek. "Human LLT1, a ligand for NKR-P1, and its variability under various conditions." Acta Crystallographica Section A Foundations and Advances 71, a1 (August 23, 2015): s265—s266. http://dx.doi.org/10.1107/s2053273315095959.

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14

Kumar, N., A. Mroz, M. Aletrari, R. Goldin, and M. Purbhoo. "PTU-121 Llt1 Is Upregulated In Hepatocellular Carcinoma And Inhibits Nk Cell Cytotoxicity." Gut 63, Suppl 1 (June 2014): A92.1—A92. http://dx.doi.org/10.1136/gutjnl-2014-307263.195.

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15

Llibre, Alba, Constantino López-Macías, Teresa Marafioti, Hema Mehta, Amy Partridge, Carina Kanzig, Felice Rivellese, et al. "LLT1 and CD161 Expression in Human Germinal Centers Promotes B Cell Activation and CXCR4 Downregulation." Journal of Immunology 196, no. 5 (February 1, 2016): 2085–94. http://dx.doi.org/10.4049/jimmunol.1502462.

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16

Kumar, Naveenta, Fouzia Sadiq, Sujit Mukherjee, Wafa Khamri, Fanny Lebossé, Ameet Dhar, Marco Purbhoo, et al. "PS-027-The LLT1-CD161 interaction: An important inhibitory interaction for NK cells in cirrhosis." Journal of Hepatology 70, no. 1 (April 2019): e20-e21. http://dx.doi.org/10.1016/s0618-8278(19)30033-7.

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Skálová, Tereza, Jan Bláha, Karl Harlos, Jarmila Dušková, Tomáš Koval', Jan Stránský, Jindřich Hašek, Ondřej Vaněk, and Jan Dohnálek. "Changes of LLT1, a ligand for human NKR-P1, with varied glycosylation and crystallization conditions." Acta Crystallographica Section A Foundations and Advances 72, a1 (August 28, 2016): s340. http://dx.doi.org/10.1107/s2053273316094936.

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18

Skalova, Tereza, Jan Bláha, Jan Stránský, Tomáš Koval, Jarmila Dušková, Yuguang Zhao, Karl Harlos, Ondřej Vaněk, and Jan Dohnálek. "Structure of human natural killer cell receptor NKR-P1 in complex with its ligand LLT1." Acta Crystallographica Section A Foundations and Advances 74, a2 (August 22, 2018): e225-e225. http://dx.doi.org/10.1107/s2053273318091775.

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19

MALAER, JOSEPH D., and PORUNELLOOR A. MATHEW. "Role of LLT1 and PCNA as Natural Killer Cell Immune Evasion Strategies of HCT 116 Cells." Anticancer Research 40, no. 12 (December 2020): 6613–21. http://dx.doi.org/10.21873/anticanres.14686.

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20

Bambard, N. D., S. O. Mathew, and P. A. Mathew. "LLT1-mediated Activation of IFN-γ Production in Human Natural Killer Cells Involves ERK Signalling Pathway." Scandinavian Journal of Immunology 71, no. 3 (March 2010): 210–19. http://dx.doi.org/10.1111/j.1365-3083.2009.02367.x.

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21

Braud, Véronique M., Jérôme Biton, Etienne Becht, Samantha Knockaert, Audrey Mansuet-Lupo, Estelle Cosson, Diane Damotte, et al. "Expression of LLT1 and its receptor CD161 in lung cancer is associated with better clinical outcome." OncoImmunology 7, no. 5 (January 29, 2018): e1423184. http://dx.doi.org/10.1080/2162402x.2017.1423184.

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22

Skalova, Tereza, Jan Blaha, Jan Stransky, Tomáš Koval, Jarmila Duskova, Ondrej Skorepa, Barbora Kalousková, Samuel Pazicky, Ondrej Vanek, and Jan Dohnálek. "SEC-SAXS analysis of oligomeric states of human NKR-P1 with its ligand LLT1 in solution." Acta Crystallographica Section A Foundations and Advances 75, a2 (August 18, 2019): e62-e62. http://dx.doi.org/10.1107/s2053273319094944.

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23

Spreu, Jessica, Eike C. Kienle, Birgit Schrage, and Alexander Steinle. "CLEC2A: a novel, alternatively spliced and skin-associated member of the NKC-encoded AICL–CD69–LLT1 family." Immunogenetics 59, no. 12 (November 29, 2007): 903–12. http://dx.doi.org/10.1007/s00251-007-0263-1.

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24

Satkunanathan, S., N. Kumar, M. Bajorek, M. A. Purbhoo, F. J. Culley, and D. Lyles. "Respiratory Syncytial Virus Infection, TLR3 Ligands, and Proinflammatory Cytokines Induce CD161 Ligand LLT1 Expression on the Respiratory Epithelium." Journal of Virology 88, no. 5 (December 18, 2013): 2366–73. http://dx.doi.org/10.1128/jvi.02789-13.

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25

Kita, Shunsuke, Haruki Matsubara, Yoshiyuki Kasai, Takaharu Tamaoki, Yuki Okabe, Hideo Fukuhara, Jun Kamishikiryo, et al. "Crystal structure of extracellular domain of human lectin-like transcript 1 (LLT1), the ligand for natural killer receptor-P1A." European Journal of Immunology 45, no. 6 (April 28, 2015): 1605–13. http://dx.doi.org/10.1002/eji.201545509.

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26

Rosen, David B., Wei Cao, Danielle T. Avery, Stuart G. Tangye, Yong-Jun Liu, J. P. Houchins, and Lewis L. Lanier. "Functional Consequences of Interactions between Human NKR-P1A and Its Ligand LLT1 Expressed on Activated Dendritic Cells and B Cells." Journal of Immunology 180, no. 10 (May 3, 2008): 6508–17. http://dx.doi.org/10.4049/jimmunol.180.10.6508.

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27

Germain, Claire, Anders Meier, Teis Jensen, Perrine Knapnougel, Gwenola Poupon, Anne Lazzari, Anne Neisig, et al. "Induction of Lectin-like Transcript 1 (LLT1) Protein Cell Surface Expression by Pathogens and Interferon-γ Contributes to Modulate Immune Responses." Journal of Biological Chemistry 286, no. 44 (September 19, 2011): 37964–75. http://dx.doi.org/10.1074/jbc.m111.285312.

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28

Santos-Juanes, J., I. Fernández-Vega, S. Lorenzo-Herrero, C. Sordo-Bahamonde, P. Martínez-Camblor, J. M. García-Pedrero, B. Vivanco, et al. "Lectin-like transcript 1 (LLT1) expression is associated with nodal metastasis in patients with head and neck cutaneous squamous cell carcinoma." Archives of Dermatological Research 311, no. 5 (April 6, 2019): 369–76. http://dx.doi.org/10.1007/s00403-019-01916-x.

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Sanchez-Canteli, Mario, Francisco Hermida-Prado, Christian Sordo-Bahamonde, Irene Montoro-Jiménez, Esperanza Pozo-Agundo, Eva Allonca, Aitana Vallina-Alvarez, et al. "P-18 Lectin-Like Transcript 1 (LLT1) expression emerges as an Independent Prognostic Factor in HPV-Negative Oropharyngeal Squamous Cell Carcinoma." Oral Oncology 118 (July 2021): 8. http://dx.doi.org/10.1016/s1368-8375(21)00307-9.

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Bláha, Jan, Petr Pachl, Petr Novák, and Ondřej Vaněk. "Expression and purification of soluble and stable ectodomain of natural killer cell receptor LLT1 through high-density transfection of suspension adapted HEK293S GnTI− cells." Protein Expression and Purification 109 (May 2015): 7–13. http://dx.doi.org/10.1016/j.pep.2015.01.006.

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Fu, Pin-I., Po-Chiung Fang, Ren-Wen Ho, Tsai-Ling Chao, Wan-Hua Cho, Hung-Yin Lai, Yu-Ting Hsiao, and Ming-Tse Kuo. "Determination of Tear Lipid Film Thickness Based on a Reflected Placido Disk Tear Film Analyzer." Diagnostics 10, no. 6 (May 28, 2020): 353. http://dx.doi.org/10.3390/diagnostics10060353.

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This study aims at determining the thickness of the tear lipid layer (LL) observed from a placido-disc-based tear film analyzer. We prospectively collected reflections of placido-disk LL images using a tear film analyzer (Keratograph® 5M, Oculus) from subjects with dry eye symptoms. The LL thickness (LLT) over the inferior half of the cornea was estimated with the use of interference color analysis and the preprocessing of images with and without ring segmentation were obtained and analyzed. Moreover, LLTs before and after 1 h of applying topical ointment (Duratears, Alcon) were compared to validate the estimation of LLT. Our results suggested that the tear LLT can be assessed using a placido-disk-based tear film analyzer and interference color analysis. We verified a high correlation between non-segmented and segmented LL images and estimated LLT increase after applying ointment. In addition, we concluded that LLT can be evaluated by direct interference analysis without segmentation preprocessing.

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Vaněk, Ondřej, Jan Bláha, Petr Pachl, and Petr Novák. "High-density transfection is superior for production of readily crystallizable glycoproteins in suspension adapted HEK293S GnTI−cells: a case study of human lymphocyte receptor LLT1." Acta Crystallographica Section A Foundations and Advances 71, a1 (August 23, 2015): s220. http://dx.doi.org/10.1107/s2053273315096680.

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Han, Chunchao, and Bo Cui. "Improvement of the Bioavailability and Glycaemic Metabolism of Cinnamon Oil in Rats by Liquid Loadable Tablets." Scientific World Journal 2012 (2012): 1–6. http://dx.doi.org/10.1100/2012/681534.

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The purpose of this study is to investigate the bioavailability and glycaemic metabolism of cinnamon oil (CIO) carried by liquid-loadable tablets (CIO-LLTs), the carrier of a CIO self-emulsifying formulation (CIO-LS). The results of tests performed to evaluate the physical properties of the CIO-LLT complied with Chinese Pharmacopeia (2010). The release profile suggested that the CIO-LLT preserved the enhancement of in vitro dissolution of cio. After orally administration, the plasma concentration-time profile and pharmacokinetic parameters suggested that a significant increase (P<0.0001) in theCmax, AUC andFwere observed in the CIO-LLT. The blood glucose and the HbA1c were significantly decreased in alloxan-induced hyperglycemic rats (P<0.05,P<0.01, resp.), while the level of insulin secretion was markedly elevated in alloxan-induced hyperglycemic rats (P<0.05). The alloxan-damaged pancreaticβ-cells of the rats were partly recovered gradually after the rats were administered with CIO-LLT 45 days later. CIO-LLT could improve the bioavailability and glycaemic metabolism of CIO.

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Danchin, Nicolas, Wael Almahmeed, Khalid Al-Rasadi, Joseph Azuri, Abdelkrim Berrah, Carlos Alberto Cuneo, Yuri Karpov, et al. "Achievement of low-density lipoprotein cholesterol goals in 18 countries outside Western Europe: The International ChoLesterol management Practice Study (ICLPS)." European Journal of Preventive Cardiology 25, no. 10 (May 17, 2018): 1087–94. http://dx.doi.org/10.1177/2047487318777079.

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Background Little is known about the achievement of low density lipoprotein cholesterol (LDL-C) targets in patients at cardiovascular risk receiving stable lipid-lowering therapy (LLT) in countries outside Western Europe. Methods This cross-sectional observational study was conducted in 452 centres (August 2015−August 2016) in 18 countries in Eastern Europe, Asia, Africa, the Middle East and Latin America. Patients ( n = 9049) treated for ≥3 months with any LLT and in whom an LDL-C measurement on stable LLT was available within the previous 12 months were included. Results The mean±SD age was 60.2 ± 11.7 years, 55.0% of patients were men and the mean ± SD LDL-C value on LLT was 2.6 ± 1.3 mmol/L (101.0 ± 49.2 mg/dL). At enrolment, 97.9% of patients were receiving a statin (25.3% on high intensity treatment). Only 32.1% of the very high risk patients versus 51.9% of the high risk and 55.7% of the moderate risk patients achieved their LDL-C goals. On multivariable analysis, factors independently associated with not achieving LDL-C goals were no (versus lower dose) statin therapy, a higher (versus lower) dose of statin, statin intolerance, overweight and obesity, female sex, neurocognitive disorders, level of cardiovascular risk, LDL-C value unknown at diagnosis, high blood pressure and current smoking. Diabetes was associated with a lower risk of not achieving LDL-C goals. Conclusions These observational data suggest that the achievement of LDL-C goals is suboptimal in selected countries outside Western Europe. Efforts are needed to improve the management of patients using combination therapy and/or more intensive LLTs.

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Ferrières, Jean, Victoria Banks, Demetris Pillas, Francesco Giorgianni, Laurene Gantzer, Beranger Lekens, Lea Ricci, et al. "Screening and treatment of familial hypercholesterolemia in a French sample of ambulatory care patients: A retrospective longitudinal cohort study." PLOS ONE 16, no. 8 (August 2, 2021): e0255345. http://dx.doi.org/10.1371/journal.pone.0255345.

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Background and aims Untreated Familial Hypercholesterolemia (FH) leads to premature morbidity and mortality. In France, its epidemiology and management are understudied in ambulatory care. We described the clinical profile, pharmacological management, and clinical outcomes in a French sample of FH patients. Methods This was a retrospective longitudinal study on patients from The Health Improvement Network (THIN®) database in France, between October 2016-June 2019. Patients ≥18 years, with probable/definite FH based on the Dutch Lipid Clinic Network (DLCN) criteria were included. Baseline characteristics, lipid profile, lipid-lowering therapy (LLT), low-density lipoprotein-cholesterol (LDL-C) goal achievement; and disease management at 6-month of follow-up were analyzed. Results 116 patients with probable (n = 70)/definite (n = 46) FH were included (mean age:57.8±14.0 years; 56.0% women; 9.5% with personal history of cardiovascular events); 90 patients had data available at follow-up. At baseline, 77.6% of patients had LDL-C>190 mg/dL, 27.6% were not receiving LLTs, 37.9% received statins alone, 20.7% statins with other LLTs, and 7.7% other LLTs. High-intensity statins were prescribed to 11.2% of patients, 30.2% received moderate-intensity statins, and 8.6% low-intensity statins. Only 6.0% of patients achieved LDL-C goal. At 6-month of follow-up, statins discontinuation and switching were 22.7% and 2.3%, respectively. None of the patients received proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors at baseline nor follow-up. Conclusions Despite the existence of effective LLTs, FH patients are suboptimally-treated, do not achieve LDL-C goal, and exhibit worsened pharmacological management over time. Future studies with longer follow-up periods and assessment of factors affecting LDL-C management, including lifestyle and diet, are needed.

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Pankratz, David. "LLTI Highlights." IALLT Journal of Language Learning Technologies 26, no. 3 (October 15, 1993): 129–32. http://dx.doi.org/10.17161/iallt.v26i3.9517.

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Pankratz, David. "LLTI Highlights." IALLT Journal of Language Learning Technologies 27, no. 1 (January 15, 1994): 69–73. http://dx.doi.org/10.17161/iallt.v27i1.9535.

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Pankratz, David. "LLTI Highlights." IALLT Journal of Language Learning Technologies 27, no. 2 (April 15, 1994): 103–8. http://dx.doi.org/10.17161/iallt.v27i2.9554.

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Pankratz, David, and Wendy B. Davis. "LLTI Highlights." IALLT Journal of Language Learning Technologies 27, no. 3 (February 18, 2019): 91–98. http://dx.doi.org/10.17161/iallt.v27i3.9569.

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Pankratz, David. "LLTI Highlights." IALLT Journal of Language Learning Technologies 28, no. 1 (February 18, 2019): 89–94. http://dx.doi.org/10.17161/iallt.v28i1.9584.

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Pankratz, David. "LLTI Highlights." IALLT Journal of Language Learning Technologies 28, no. 2 (February 18, 2019): 79–87. http://dx.doi.org/10.17161/iallt.v28i2.9597.

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Pankratz, David. "LLTI Highlights." IALLT Journal of Language Learning Technologies 29, no. 1 (January 1, 1996): 59–70. http://dx.doi.org/10.17161/iallt.v29i1.9610.

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Pankratz, David. "LLTI Highlights." IALLT Journal of Language Learning Technologies 29, no. 2 (April 1, 1996): 49–56. http://dx.doi.org/10.17161/iallt.v29i2.9625.

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Pankratz, David. "LLTI Highlights." IALLT Journal of Language Learning Technologies 29, no. 3 (October 1, 1996): 37–44. http://dx.doi.org/10.17161/iallt.v29i3.9636.

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Pankratz, David. "LLTI Highlights." IALLT Journal of Language Learning Technologies 30, no. 1 (January 1, 1997): 79–90. http://dx.doi.org/10.17161/iallt.v30i1.9653.

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Pankratz, David. "LLTI Highlights." IALLT Journal of Language Learning Technologies 30, no. 2 (February 1, 1998): 41–48. http://dx.doi.org/10.17161/iallt.v30i2.9666.

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Pankratz, David. "LLTI Highlights." IALLT Journal of Language Learning Technologies 30, no. 3 (June 1, 1998): 55–64. http://dx.doi.org/10.17161/iallt.v30i3.9680.

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Berger, Michael, and Barbara Need. "LLTI Highlights." IALLT Journal of Language Learning Technologies 31, no. 1-2 (February 1, 1999): 73–78. http://dx.doi.org/10.17161/iallt.v31i1-2.9695.

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Berger, Michael, and Barbara Need. "LLTI Highlights." IALLT Journal of Language Learning Technologies 31, no. 3 (April 1, 1999): 69–76. http://dx.doi.org/10.17161/iallt.v31i3.9707.

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Lahaie, Ute S. "LLTI Highlights." IALLT Journal of Language Learning Technologies 33, no. 2 (October 15, 2001): 75–84. http://dx.doi.org/10.17161/iallt.v33i2.8338.

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