Relevant bibliographies by topics / Targeting Mice

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Targeting Mice'

Author: Grafiati
Published: 29 July 2024
Last updated: 31 July 2024

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Journal articles on the topic "Targeting Mice"

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Gogos, Joseph A., and Maria Karayiorgou. "?Targeting? schizophrenia in mice." American Journal of Medical Genetics 105, no. 1 (2001): 50–52. http://dx.doi.org/10.1002/1096-8628(20010108)105:1<50::aid-ajmg1058>3.0.co;2-5.

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Kuhn, R., F. Schwenk, M. Aguet, and K. Rajewsky. "Inducible gene targeting in mice." Science 269, no. 5229 (September 8, 1995): 1427–29. http://dx.doi.org/10.1126/science.7660125.

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Gao, Jiangang, Xudong Wu, and Jian Zuo. "Targeting hearing genes in mice." Molecular Brain Research 132, no. 2 (December 2004): 192–207. http://dx.doi.org/10.1016/j.molbrainres.2004.06.035.

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Bléry, Mathieu, Manel Mrabet-Kraiem, Ariane Morel, Florence Lhospice, Delphine Bregeon, Cécile Bonnafous, Laurent Gauthier, et al. "Targeting MICA/B with cytotoxic therapeutic antibodies leads to tumor control." Open Research Europe 1 (October 27, 2021): 107. http://dx.doi.org/10.12688/openreseurope.13314.2.

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Background: MICA and MICB are tightly regulated stress-induced proteins that trigger the immune system by binding to the activating receptor NKG2D on cytotoxic lymphocytes. MICA and MICB are highly polymorphic molecules with prevalent expression on several types of solid tumors and limited expression in normal/healthy tissues, making them attractive targets for therapeutic intervention. Methods: We have generated a series of anti-MICA and MICB cross-reactive antibodies with the unique feature of binding to the most prevalent isoforms of both these molecules. Results: The anti-MICA and MICB antibody MICAB1, a human IgG1 Fc-engineered monoclonal antibody (mAb), displayed potent antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP) of MICA/B-expressing tumor cells in vitro. However, it showed insufficient efficiency against solid tumors in vivo, which prompted the development of antibody-drug conjugates (ADC). Indeed, optimal tumor control was achieved with MICAB1-ADC format in several solid tumor models, including patient-derived xenografts (PDX) and carcinogen-induced tumors in immunocompetent MICAgen transgenic mice. Conclusions: These data indicate that MICA and MICB are promising targets for cytotoxic immunotherapy.
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Bléry, Mathieu, Manel Mrabet-Kraiem, Ariane Morel, Florence Lhospice, Delphine Bregeon, Cécile Bonnafous, Laurent Gauthier, et al. "Targeting MICA/B with cytotoxic therapeutic antibodies leads to tumor control." Open Research Europe 1 (September 13, 2021): 107. http://dx.doi.org/10.12688/openreseurope.13314.1.

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Background: MICA and MICB are tightly regulated stress-induced proteins that trigger the immune system by binding to the activating receptor NKG2D on cytotoxic lymphocytes. MICA and MICB are highly polymorphic molecules with prevalent expression on several types of solid tumors and limited expression in normal/healthy tissues, making them attractive targets for therapeutic intervention. Methods: We have generated a series of anti-MICA and MICB cross-reactive antibodies with the unique feature of binding to the most prevalent isoforms of both these molecules. Results: The anti-MICA and MICB antibody MICAB1, a human IgG1 Fc-engineered monoclonal antibody (mAb), displayed potent antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP) of MICA/B-expressing tumor cells in vitro. However, it showed insufficient efficiency against solid tumors in vivo, which prompted the development of antibody-drug conjugates (ADC). Indeed, optimal tumor control was achieved with MICAB1-ADC format in several solid tumor models, including patient-derived xenografts (PDX) and carcinogen-induced tumors in immunocompetent MICAgen transgenic mice. Conclusions: These data indicate that MICA and MICB are promising targets for cytotoxic immunotherapy.
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Chen, Szu-Tah, Shin-Huei Fu, Samuel Hsu, Yu-Yao Huang, and Brend Ray-Sea Hsu. "Synergistic Effect of Hyperglycemia and Suppression on Adult Mouse Islet Beta Cell Replication." International Journal of Endocrinology 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/417390.

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The complementary role of hyperglycemia and suppression on islet beta cell regeneration was investigated in a syngeneic mouse model. gene silencing was performed by infecting islets of C57BL/6 with shRNA lentiviral particles. At 54 hours after viral infection, protein content in cultured targeting islets was 22% of that in freshly isolated islets. Six days after transplantation to diabetic mice, targeting islet graft had considerably more cells with Ki67-staining nuclei than nontargeting islets. The mice in the targeting-islet group had a significantly shorter duration of temporary hyperglycaemia than mice in the non-targeting-islet group. The long-termex vivobeneficial effect of silencing on graft function was also indicated by the significantly higher cumulative cure rate for diabetes in mice receiving 200 targeting islets than that in mice receiving 200 non-targeting islets. Our data suggest that hyperglycemia and persistent suppression have a synergistic effect on islet beta cell replication in adult mice.
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Nakamura, K., C. Fan, G. Liu, S. Gupta, J. He, S. Dou, A. Kubo, M. Rusckowski, and D. J. Hnatowich. "Evidence of Antisense Tumor Targeting in Mice." Bioconjugate Chemistry 15, no. 6 (November 2004): 1475–80. http://dx.doi.org/10.1021/bc0499073.

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Wu, Lawren C., and Heleen Scheerens. "Targeting IgE production in mice and humans." Current Opinion in Immunology 31 (December 2014): 8–15. http://dx.doi.org/10.1016/j.coi.2014.08.001.

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Collison, Joanna. "Targeting Bcl-2 prevents nephritis in mice." Nature Reviews Rheumatology 12, no. 7 (May 26, 2016): 376. http://dx.doi.org/10.1038/nrrheum.2016.90.

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M. Gordon, Erlinda, Seiya Liu, Sant P. Chawla, and Frederick L. Hall. "Polypeptidic Taxol-Tropins: Targeting paclitaxel to the tumor microenvironment." Cancer Research and Cellular Therapeutics 5, no. 3 (July 26, 2021): 01–11. http://dx.doi.org/10.31579/2640-1053/089.

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Background and Rationale: Although PTX is widely used as a single chemotherapeutic agent and in various combination regimens, its clinical utility is hindered by acquired drug resistance and serious dose-limiting side effects that result from the ungoverned biodistribution of the taxane. Hypothesis: Conceptually, the precision, validity, and efficiency of paclitaxel delivery to tumor compartments might be substantially improved by “actively targeting” the exposed collagenous (XC-) proteins presented within the tumor microenvironment (TME)—XC-proteins physically exposed by the pathologic biochemical processes of tumor invasion, reactive stroma formation, and neo-angiogenesis. Objective: An adaptive bioengineering approach aims to apply pathotropic tumor-targeting functionality to paclitaxel (PTX), a powerful cytotoxic taxane which exhibits anti-tubulin / anti-mitotic / anti-cancer activities against a broad range of solid tumors. Materials and Methods: Synthetic peptide XC-targeting probes (< 40 aa) and polypeptide aptamers (40 to 53 aa), 85 - 99% purity, were prepared by 9-fluorenylmethyloxycarbonyl (Fmoc) solid phase peptide synthesis, purified by high performance liquid chromatography (HPLC), and verified by mass spectrometry and amino acid analysis, and the XC-targeting probes were FITC-labeled. Analysis of fluorescence in XC-binding assays was visualized with an Ultra Bright Blue Light trans-illuminator equipped with an amber filter; photo-documentation was provided by a Leica V-Lux 1 digital camera; and comparative fluorescence was quantified using a Quantus benchtop fluorimeter (Promega). The tumor-targeting properties of Taxol-Tropins were tested in vitro by Taxol-aptamer binding assays and collagen-agarose binding assays and the bioactivities of PTX bound non-covalently toTaxol-Tropin aptamers were tested on XC-agarose beads. Further, the tumor targeting property of the Taxol-Tropin aptamers was tested in vivo in a murine model of metastatic cancer. Results: Here we report on the first actively targeted delivery of paclitaxel utilizing bifunctional polypeptide targeting onco-aptamers, called Taxol-Tropins, which: (i) bind PTX upon simple mixing with suitably high affinities and; (ii) bind exposed XC-proteins, thereby promoting enhanced partitioning and drug delivery into the TME. The bifunctional peptide sequence-optimized Taxol-Tropins bound tightly non-covalently to PTX and also exhibited high affinity and selectivity for XC-agarose beads in vitro. Importantly, the cytotoxic bioactivity of the Taxol-Tropin-bound-PTX molecule was well preserved in cellulo, as was demonstrated by cytocidal activity observed in MDA-MB-231 breast cancer cell cultures. Tumor-targeted PTX delivery by Taxol-Tropin onco-aptamers in vivo was modeled by subcutaneous xenografts of human pancreatic cancer in nude mice: where intense fluorescence of the PTX probe was observed in tumors of mice injected with the Taxol-Tropin-bound-PTX within minutes after intravenous injection, but not in untreated mice or mice treated with non-targeted PTX probe. Conclusions: These results demonstrate the feasibility of pro-actively targeting PTX, a clinically important small molecule, using Taxol-Tropins: synthetic polypeptide onco-aptamers, revealing optimized drug binding sequences and structural modifications pertinent to further clinical development of the tumor-targeting platform which may indeed shift the Therapeutic Index of PTX to one of greater clinical efficacy at lower drug doses.
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Dissertations / Theses on the topic "Targeting Mice"

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Shelton, Laura Marie. "Targeting Energy Metabolism in Brain Cancer." Thesis, Boston College, 2010. http://hdl.handle.net/2345/1183.

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Thesis advisor: Thomas N. Seyfried
It has long been posited that all cancer cells are dependent on glucose for energy, termed the "Warburg Effect". As a result of an irreversible injury to the mitochondria, cancer cells are less efficient in aerobic respiration. Therefore, calorie restriction was thought to be a natural way to attenuate tumor growth. Calorie restriction lowers blood glucose, while increasing the circulation of ketone bodies. Ketone bodies are metabolized via oxidative phosphorylation in the mitochondria. Only cells that are metabolically capable of aerobic respiration will thus be able to acquire energy from ketone bodies. To date, calorie restriction has been shown to greatly reduce tumor growth and angiogenesis in the murine CT2A, EPEN, and human U87 brain tumor models. Using the novel VM-M3 model for invasive brain cancer and systemic metastatic cancer, I found that though calorie restriction had some efficacy in reducing brain tumor invasion and primary tumor size, metastatic spread was unaffected. Using a bioluminescent-based ATP assay, I determined the viability of metastatic mouse VM-M3 tumor cells grown in vitro in serum free medium in the presence of glucose alone (25 mM), glutamine alone (4 mM), or in glucose + glutamine. The VM-M3 cells could not survive on glucose alone, but could survive in glutamine alone indicating an absolute requirement for glutamine in these metastatic tumor cells. Glutamine could also maintain viability in the absence of glucose and in the presence of the F1 ATPase inhibitor oligomycin. Glutamine could not maintain viability in the presence of the Krebs (TCA) cycle enzyme inhibitor, 3-nitropropionic acid. The data indicate that glutamine can provide ATP for viability in the metastatic VM-M3 cells through Krebs cycle substrate level phosphorylation in the absence of energy from either glycolysis or oxidative phosphorylation. I therefore developed a metabolic therapy that targeted both glucose and glutamine metabolism using calorie restriction and 6-diazo-5-oxo-L-norleucine (DON), a glutamine analog. Primary tumor growth was about 20-fold less in DON treated mice than in untreated control mice. I also found that DON treatment administered alone or in combination with CR inhibited metastasis to liver, lung, and kidney as detected by bioluminescence imaging and histology. Although DON treatment alone did not reduce the incidence of tumor metastasis to spleen compared to the controls, DON administered together with CR significantly reduced the incidence of metastasis to the spleen, indicating a diet/drug synergy. In addition, the phagocytic capabilities of the VM-M3 tumor cells were enhanced during times of energy stress. This allowed for the digestion of engulfed material to be used in energy production. My data provide proof of concept that metabolic therapies targeting both glucose and glutamine metabolism can manage systemic metastatic cancer. Additionally, due to the phagocytic properties of the VM-M3 cell line also seen in a number of human metastatic cancers, I suggest that a unique therapy targeting metabolism and phagocytosis will be required for effective management of metastatic cancer
Thesis (PhD) — Boston College, 2010
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Biology
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Lu, Linyu. "Investigations into the feasibility of single-stranded oligonucleotide-mediated targeted gene repair in mammalian cells." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B37552636.

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Tsang, Wai-hung, and 曾偉雄. "Studying the roles of mouse Sox10 by conditional gene targeting." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B3124483X.

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Lu, Linyu, and 陸林宇. "Investigations into the feasibility of single-strandedoligonucleotide-mediated targeted gene repair in mammalian cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B38722793.

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Wong, Kung-yen Corinne, and 黃共欣. "Analysis of abnormal phenotypes of Hoxb3 mouse mutants generated by gene targeting." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29158904.

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Benn, Caroline Louise. "Targeting mutant huntingtin to the nucleus accelerates phenotype onset in transgenic mice." Thesis, King's College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.401268.

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Thompson, Simon. "The study of HPRT gene expression using gene targeting and transgenic mice." Thesis, University of Edinburgh, 1989. http://hdl.handle.net/1842/13115.

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Ledin, Johan. "Heparan Sulfate Biosynthesis – Clues from Knockout Mice." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3992.

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Yang, Li. "Studying the Function of Rho Family GTPase Cdc42 by Gene Targeting in Mice." University of Cincinnati / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1172690084.

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Curry, Zachary. "Targeting monoacylglycerol lipase for the reversal and prevention of paclitaxel-induced allodynia in mice." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5274.

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Chemotherapy-induced peripheral neuropathy (CIPN) is a side-effect of chemotherapy causing pain in the hands and feet. In particular, paclitaxel causes CIPN lasting for years without effective treatment. There is a strong need for analgesics to both treat and prevent CIPN. One system containing multiple targets to treat CIPN is the endogenous cannabinoid system. This system consists of cannabinoid type 1 (CB1) and type 2 (CB2) receptors primarily expressed on presynaptic neurons and cells of the immune system, respectively. Inhibition of monoacylglycerol lipase (MAGL), which hydrolyzes the endogenous cannabinoid 2- arachidonoylglycerol (2-AG), with JZL184 or MJN110 produces antinociceptive and anti- inflammatory effects in rodent pain models. In this dissertation, we test the hypothesis that MAGL inhibitors will both reverse and prevent mouse paclitaxel-induced mechanical allodynia. JZL184 and MJN110 reversed paclitaxel allodynia in dose-dependent manners with ED50 values (95% C.L.) of 8.4 (5.2-13.6) and 1.8 (1.0-3.3) mg/kg. Using genetic and pharmacologic approaches, we demonstrate that the anti-allodynic effects of both inhibitors require both cannabinoid receptors. As CIPN treatment could require repeated dosing, we demonstrate that repeated administration of 4 mg/kg JZL184 for six days produces anti-allodynic effects in contrast to tolerance development after repeated treatment with 40 mg/kg. We also show that MJN110 attenuates paclitaxel-induced inflammation in the spinal cord and dorsal root ganglia (DRG), namely monocyte chemoattractant protein-1 (MCP-1, CCL2) and phosphorylated p38 MAPK (phospho-p38) expression. Using the conditioned place preference (CPP) paradigm, we demonstrate that MJN110 produces a CPP in paclitaxel-treated, but not in control mice. As CIPN develops during chemotherapy, we also show that JZL184 does not interfere with the anti- proliferative and anti-apoptotic effects of paclitaxel in A549 or H460 lung cancer cell lines. Lastly, we show that co-administration of MAGL inhibitors with paclitaxel prevents the development of allodynia. Co-treatment with 5 mg/kg MJN110 or 40 mg/kg JZL184 prevents allodynia up to one or two week(s), respectively, after paclitaxel cessation. Treatment with 40 mg/kg JZL184 prevents allodynia in both CB1 (+/+) and (-/-) mice, suggesting that prevention is CB1-independent. Taken together, these results suggest that MAGL is a viable target for both the treatment and prevention of paclitaxel-induced allodynia in mice.
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Books on the topic "Targeting Mice"

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L, Joyner Alexandra, ed. Gene targeting: A practical approach. Oxford: IRL Press at Oxford University Press, 1993.

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1955-, Wurst Wolfgang, ed. Gene knockout protocols. 2nd ed. New York, NY: Humana Press, 2009.

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Kühn, Ralf. Gene knockout protocols. 2nd ed. New York, NY: Humana Press, 2009.

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Durum, Scott K., and Kathrin Muegge. Cytokine Knockouts. Humana Press, 2013.

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Tymms, Martin J., and Ismail Kola. Gene Knockout Protocols. Humana Press, 2010.

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(Editor), Martin J. Tymms, and Ismail Kola (Editor), eds. Gene Knockout Protocols (Methods in Molecular Biology). Humana Press, 2001.

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Gene Knockout Protocols. Humana Press, 2004.

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Fantuzzi, Giamila. Cytokine Knockouts. Humana Press, 2010.

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Wurst, Wolfgang, and Ralf Kühn. Gene Knockout Protocols. Humana Press, 2014.

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Khachatryan, Armen. Targeting of calcitonin gene-related peptide expression to the pancreatic beta cells prevents insulin-dependent diabetes mellitus in non-obese diabetic mice. 1996.

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Book chapters on the topic "Targeting Mice"

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Shi, Jiayuan, Li Hua, Danielle Harmer, Peishan Li, and Guangwen Ren. "Cre Driver Mice Targeting Macrophages." In Macrophages, 263–75. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7837-3_24.

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Bouabe, Hicham, and Klaus Okkenhaug. "Gene Targeting in Mice: A Review." In Methods in Molecular Biology, 315–36. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-601-6_23.

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Gabizon, A., S. K. Huang, and D. Papahadjopoulos. "Sterically Stabilized Liposomes as Drug Carriers: Pharmacokinetics, Tissue Distribution and Therapeutic Effects in Tumour-Bearing Mice." In Targeting of Drugs 3, 51–58. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-2938-5_6.

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Brandau, O., and R. Fässler. "Analysis of Integrin Function by Gene Targeting in Mice." In Transgenic Models in Pharmacology, 193–225. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18934-0_7.

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Turunen, Tiia A., Seppo Ylä-Herttuala, and Mikko P. Turunen. "Enhancing Angiogenesis in Mice by VEGF-Targeting Small Activating RNAs." In RNA Activation, 195–205. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4310-9_14.

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Wei, Dongping, and Lijun Jia. "Oral Delivery of Tumor-Targeting Salmonella to Treat Cancer in Mice." In Methods in Molecular Biology, 25–33. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3515-4_3.

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Passananti, Claudio, Nicoletta Corbi, Annalisa Onori, Maria Grazia Di Certo, and Elisabetta Mattei. "Transgenic Mice Expressing an Artificial Zinc Finger Regulator Targeting an Endogenous Gene." In Methods in Molecular Biology, 183–206. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-753-2_11.

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Bremer, Jeroen, and Peter C. van den Akker. "In Vivo Models for the Evaluation of Antisense Oligonucleotides in Skin." In Methods in Molecular Biology, 315–20. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2010-6_21.

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AbstractHere, we describe an in vivo model in which antisense oligonucleotides were preclinically evaluated in reconstituted patient and healthy control skin. The aim was to investigate the effect of antisense oligonucleotides upon local or systemic administration. This allows for clinically relevant evaluation of antisense oligonucleotides in an in vivo setting. In this model, primary human keratinocytes and fibroblasts were placed into silicone grafting chambers, implanted onto the back of athymic nude mice. After sufficient cells were expanded, within a few weeks, human skin grafts were generated with a high success rate. These mice bearing grafts were subsequently treated with antisense oligonucleotides targeting exon 105 of the COL7A1 gene which encodes type VII collagen. Patients completely lacking expression of type VII collagen develop severe blistering of skin and mucosa, i.e., recessive dystrophic epidermolysis bullosa. In this chapter, we describe the in vivo model used for the preclinical evaluation of antisense oligonucleotides as therapeutic approach for recessive dystrophic epidermolysis bullosa.
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Mak, Tak W., Amin Rahemtulla, Marco Schilham, Dow Rhoon Koh, and Wai Ping Fung-Leung. "Generation of Mutant Mice Lacking Surface Expression of CD4 or CD8 Gene Targeting." In Advances in Experimental Medicine and Biology, 73–77. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3396-2_10.

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Sherman, L. A., M. Theobald, and J. Lustgarten. "The Use of HLA Transgenic Mice in Identifying and Targeting Human Tumor Cell Antigens." In Symposium in Immunology VI, 41–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60562-8_4.

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Conference papers on the topic "Targeting Mice"

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Schuoler, Claudio, Thomas Haider, Caroline Leuenberger, Johannes Vogel, Louise Ostergaard, Malcolm Kohler, Max Gassmann, Lars Huber, and Matthias Brock. "Targeting aquaporin 1 reverses hypoxia-induced pulmonary hypertension in mice." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa5104.

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Firestone, Ross S., Mu Feng, and Vern L. Schramm. "Abstract 18: Doubled lifespan in APCMin/+mice by targeting MTAP." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-18.

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Firestone, Ross S., Mu Feng, and Vern L. Schramm. "Abstract 18: Doubled lifespan in APCMin/+mice by targeting MTAP." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-18.

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Schloss, Kaelyn H., Xiaodan Wang, Jonah A. Padawer-Curry, Annie R. Bice, and Adam Q. Bauer. "Spatiotemporal Properties of Stimulus-evoked Responses in Mice Following Single Whisker Stimulation." In Optics and the Brain. Washington, D.C.: Optica Publishing Group, 2024. http://dx.doi.org/10.1364/brain.2024.bm5c.5.

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We used novel peripheral stimulation methods to achieve highly precise single whisker targeting to examine spatiotemporal relationships between stimulus-evoked neuronal, metabolic, and hemodynamic activity in awake mice using wide-field optical imaging.
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Rui-Zhi Zhao, You-Jun Chen, and Jian-xiong Cai. "Liver targeting effect of vinegar-baked Radix Bupleuri on oxymatrine in mice." In 2011 IEEE International Conference on Bioinformatics and Biomedicine Workshops (BIBMW). IEEE, 2011. http://dx.doi.org/10.1109/bibmw.2011.6112462.

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Gurova, Katerina V., Henry Garcia, Mairead Commane, and Alfiya Safina. "Abstract 3843: Targeting FACT complex suppresses mammary tumorigenesis in Her2/neu transgenic mice." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3843.

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Wali, S., D. Goldblatt, J. Pantaleón García, M. J. Tuvim, B. F. Dickey, and S. E. Evans. "Targeting CD8+ T Cell Immunopathology to Improve Survival of Viral Pneumonia in Mice." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3896.

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Kovar, Joy L., Evan Curtis, Shadi F. Othman, Melanie A. Simpson, and D. Michael Olive. "Abstract C4: Specific targeting of spontaneous medulloblastoma tumors in mice by IRDye 800CW chlorotoxin." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-c4.

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Yin, Yi, Xianming Huang, Dan Ye, and Philip Thorpe. "Abstract 1244: Phosphatidylserine-targeting antibody reactivates tumor immunity and destroys tumor vasculature in mice." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1244.

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Burlion, Aude, Aurélien Corneau, and Gilles Marodon. "Abstract A053: Targeting ICOS improves immune-mediated control of tumor growth in humanized mice." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-a053.

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Reports on the topic "Targeting Mice"

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McAllister, Kimberely A., and Roger Wiseman. Mammary-Specific Targeting of the BRCA2 Breast Cancer Susceptibility Gene in Mice. Fort Belvoir, VA: Defense Technical Information Center, December 1999. http://dx.doi.org/10.21236/ada390479.

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McAllister, Kimberly A., and Roger Wiseman. Mammary-Specific Targeting of the BRCA2 Breast Cancer Susceptibility Gene in Mice. Fort Belvoir, VA: Defense Technical Information Center, November 2000. http://dx.doi.org/10.21236/ada393317.

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Roy, Madhumita. Black Tea Extract prevents 4-nitroquinoline 1-oxide induced oral tumorigenesis in mice by targeting Protein Tyrosine Kinases and associated biological response. Science Repository OÜ, March 2019. http://dx.doi.org/10.31487/j.cor.2019.01.102.

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Needham, Glenn R., Uri Gerson, Gloria DeGrandi-Hoffman, D. Samatero, J. Yoder, and William Bruce. Integrated Management of Tracheal Mite, Acarapis woodi, and of Varroa Mite, Varroa jacobsoni, Major Pests of Honey Bees. United States Department of Agriculture, March 2000. http://dx.doi.org/10.32747/2000.7573068.bard.

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Abstract:
Objectives: The Israeli work plan regarding HBTM included: (a) producing a better diagnostic method; (b) following infestations during the season and evaluating damage to resistant bees and, (c) controlling HBTM by conventional means under local conditions. For varroa our plans to try novel control (e.g. oil novel control (e.g. oil patties & essential oils) were initially delayed by very low pest populations, then disrupted by the emergence of fluvalinate resistance. We monitored the spread of resistance to understand it better, and analyzed an underlying biochemical resistance mechanism in varroa. The US work plan focused on novel management methods for both mites with an emphasis on reducing use of traditional insecticides due to resistance and contamination issues. Objectives were: (a) evaluating plant essential oils for varroa control; (b) exploring the vulnerability of varroa to desiccation for their management; and (c) looking for biological variation in HBTM that could explain virulence variability between colonies. Although the initial PI at the USDA Beltsville Bee Lab, W.A. Bruce, retired during the project we made significant strides especially on varroa water balance. Subcontracts were performed by Yoder (Illinois College) on varroa water balance and DeGrandi-Hoffman (USDA) who evaluated plant essential oils for their potential to control varroa. We devised an IPM strategy for mite control i the U.S. Background: Mites that parasitize honey bees are a global problem. They are threatening the survival of managed and feral bees, the well-being of commercial/hobby beekeeping, and due to pollination, the future of some agricultural commodities is threatened. Specific economic consequences of these mites are that: (a) apiculture/breeder business are failing; (b) fewer colonies exist; (c) demand and cost for hive leasing are growing; (d) incidences of bee pathogens are increasing; and, (e) there are ore problems with commercial-reared bees. As a reflection of the continued significance f bee mites, a mite book is now in press (Webster & delaplane, 2000); and the 2nd International Conference on Africanized Honey Bees and Bee Mites is scheduled (April, 2000, Arizona). The first such conference was at OSU (1987, GRN was co-organizer). The major challenge is controlling two very different mites within a colony while not adversely impacting the hive. Colony management practices vary, as do the laws dictating acaricide use. Our basic postulates were that: (a) both mites are of economic importance with moderate to high infestations but not at low rates and, (b) once established they will not be eradicated. A novel strategy was devised that deals with the pests concomitantly by maintaining populations at low levels, without unnecessary recourse to synthetic acaricides. Major Conclusions, Solutions, Achievements: A major recent revelation is that there are several species of "Varroa jacobsoni" (Anderson & Trueman 1999). Work on control, resistance, population dynamics, and virulence awaits knowing whether this is a problem. In the U.S. there was no difference between varroa from three locales in terms of water balance parameters (AZ, MN & PA), which bodes well for our work to date. Winter varroa (U.S.) were more prone to desiccation than during other seasons. Varroa sensitivity to desiccation has important implications for improving IPM. Several botanicals showed some promise for varroa control (thymol & origanum). Unfortunately there is varroa resistance to Apistan in Israel but a resistance mechanism was detected for the first time. The Israel team also has a new method for HBTM diagnosis. Annual tracheal mite population trends in Israel were characterized, which will help in targeting treatment. Effects of HBTM on honey yields were shown. HBTM control by Amitraz was demonstrated for at least 6 months. Showing partial resistance by Buckfast bees to HBTM will be an important IPM tactic in Israel and U.S.
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