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      1. Author :
        Stavrakis, Alexandra I.; Zhu, Suwei; Hegde, Vishal; Loftin, Amanda H.; Ashbaugh, Alyssa G.; Niska, Jared A.; Miller, Lloyd S.; Segura, Tatiana; Bernthal, Nicholas M.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2016
      5. Publication :
        The Journal of Bone & Joint Surgery
      6. Products :
      7. Volume :
        98
      8. Issue :
        14
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS; IVIS BLI in vivo
      12. Abstract :
        Background: Postoperative infection is a devastating complication following arthroplasty. The goals of this study were to introduce a “smart” implant coating that combines passive elution of antibiotic with an active-release mechanism that “targets” bacteria, and to use an established in vivo mouse model of post-arthroplasty infection to longitudinally evaluate the efficacy of this polymer implant coating in decreasing bacterial burden.Methods: A novel, biodegradable coating using branched poly(ethylene glycol)-poly(propylene sulfide) (PEG-PPS) polymer was designed to deliver antibiotics both passively and actively. In vitro-release kinetics were studied using high-performance liquid chromatography (HPLC) quantification in conditions representing both the physiologic environment and the more oxidative, hyperinflammatory environment of periprosthetic infection. The in vivo efficacy of the PEG-PPS coating delivering vancomycin and tigecycline was tested using an established mouse model of post-arthroplasty infection. Noninvasive bioluminescence imaging was used to quantify the bacterial burden; radiography, to assess osseointegration and bone resorption; and implant sonication, for colony counts.Results: In vitro-release kinetics confirmed passive elution above the minimum inhibitory concentration (MIC). A rapid release of antibiotic was noted when challenged with an oxidative environment (p < 0.05), confirming a “smart” active-release mechanism. The PEG-PPS coating with tigecycline significantly lowered the infection burden on all days, whereas PEG-PPS-vancomycin decreased infection on postoperative day (POD) 1, 3, 5, and 7 (p < 0.05). A mean of 0, 9, and 2.6 × 102 colony-forming units (CFUs) grew on culture from the implants treated with tigecycline, vancomycin, and PEG-PPS alone, respectively, and a mean of 1.2 × 102, 4.3 × 103, and 5.9 × 104 CFUs, respectively, on culture of the surrounding tissue (p < 0.05).Conclusions: The PEG-PPS coating provides a promising approach to preventing periprosthetic infection. This polymer is novel in that it combines both passive and active antibiotic-release mechanisms. The tigecycline-based coating outperformed the vancomycin-based coating in this study.Clinical Relevance: PEG-PPS polymer provides a controlled, “smart” local delivery of antibiotics that could be used to prevent postoperative implant-related infections.%U http://jbjs.org/content/jbjsam/98/14/1183.full.pdf
      13. URL :
        N/A
      14. Call Number :
        PKI @ user @ 12155
      15. Serial :
        19468
      1. Author :
        Huang, Jia-Lin; Jiang, Gan; Song, Qing-Xiang; Gu, Xiao; Song, Hua-Hua; Wang, Xiao-Lin; Jiang, Di; Kang, Ting; Feng, Xing-Ye; Jiang, Xin-Guo; Chen, Hong-Zhuan; Gao, Xiao-Ling
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2016
      5. Publication :
        Die Pharmazie – An International Journal of Pharmaceutical Sciences
      6. Products :
      7. Volume :
        71
      8. Issue :
        12
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Maestro
      12. Abstract :
        Rational design of the physicochemical properties of nanocarriers can optimize their pharmacokinetics, biodistribution, intratumoral penetration and tumor bioavailability. In particular, particle shape is one of the crucial parameters that can impact the circulation time, tumor accumulation and tumor cell internalization of nanocarrier. Biomimetic reconstituted high-density lipoprotein (rHDL), by mimicking the endogenous shape and structure of high-density lipoprotein, has been indicated as a promising tumor-targeting nanoparticulate drug delivery system whereas the effect of shape on tumor-targeting efficiency has not been fully evaluated. Herein, we constructed apolipoprotein E-based biomimetic rHDL in both discoidal form (d-rHDL) and spherical form (s-rHDL), and compared their efficiency in glioblastoma multiforme (GBM)-targeting delivery. s-rHDL showed higher cellular association in GBM cells especially at a high exposure dosage or after a long incubation time. Moreover, it exhibited deeper penetration in 3D GBM spheroids in vitro and higher accumulation at the GBM site in vivo with the GBM-targeting accumulation of s-rHDL increased by 73% when compared with that of d-rHDL at 24 h post-injection. The findings collectively indicated that s-rHDL might serve as a more efficient nanocarrier for glioblastoma-targeting drug delivery.
      13. URL :
        http://www.ingentaconnect.com/content/govi/pharmaz/2016/00000071/00000012/art00004 https://doi.org/10.1691/ph.2016.6081
      14. Call Number :
        PKI @ catherine.lautenschlager @ 13033
      15. Serial :
        12961
      1. Author :
        Lv, Sihan; Qiu, Xinchen; Li, Jian; Liang, Jinye; Li, Weida; Zhang, Chao; Zhang, Zhenning; Luan, Bing
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2017
      5. Publication :
        Journal of Endocrinology
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS in vivo
      12. Abstract :
        Hormonal signals help to maintain glucose and lipid homeostasis in the liver during periods of fasting. Glucagon, a pancreas-derived hormone induced by fasting, promotes gluconeogenesis through induction of intracellular cAMP production. Glucagon also stimulates hepatic fatty acid oxidation but the underlying mechanism is poorly characterized. Here we reported that following the acute induction of gluconeogenic genes Glucose 6 phosphatase (G6Pase) and Phosphoenolpyruvate carboxykinase (Pepck) expression through CREB, glucagon triggers a second delayed phase of fatty acid oxidation genes Acyl-coenzyme A oxidase (Aox) and Carnitine palmitoyltransferase 1a (Cpt1a) expression via extracellular cAMP. Increase in extracellular cAMP promotes PPARα activity through direct phosphorylation by AMPK, while inhibition of cAMP efflux greatly attenuates Aox and Cpt1a expression. Importantly, cAMP injection improves lipid homeostasis in fasted mice and obese mice, while inhibition of cAMP efflux deteriorates hepatic steatosis in fasted mice. Collectively, our results demonstrate the vital role of glucagon-stimulated extracellular cAMP in the regulation of hepatic lipid metabolism through AMPK mediated PPARα activation. Therefore, strategies to improve cAMP efflux could serve as potential new tools to prevent obesity-associated hepatic steatosis.
      13. URL :
        http://joe.endocrinology-journals.org/content/early/2017/05/17/JOE-16-0649.abstract http://joe.endocrinology-journals.org/content/234/2/73
      14. Call Number :
        PKI @ catherine.lautenschlager @ 13905
      15. Serial :
        13905
      1. Author :
        Pennati, Andrea; Ng, Spencer; Wu, Yuanqiang; Murphy, Jordan R.; Deng, Jiusheng; Rangaraju, Srikant; Asress, Seneshaw; Blanchfield, Jennifer L.; Evavold, Brian; Galipeau, Jacques
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2016
      5. Publication :
        The Journal of Neuroscience
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS; IVIS BLI in vivo
      12. Abstract :
        Although B cells are traditionally known for their role in propagating pro-inflammatory immune responses, their immunosuppressive effects have only begun to be recently appreciated. How these regulatory B cells (Bregs) suppress the immune response remains to be worked out in detail. In this paper we show that Bregs can induce formation of conventional FoxP3+ regulatory T cells (Tregs), as well as a more recently described CD49b+CD223+ regulatory T cell subset, known as type 1 regulatory T cells (Tr1). When Bregs are transferred into mice with experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis, they home to the spleen and mesenteric lymph nodes, leading to an expansion of Tregs and Tr1 in vivo. Tregs and Tr1 cells are also found in greater proportions in the central nervous system of mice with EAE treated with Bregs and are correlated with remission of symptoms. The discovery that Bregs induce the formation of regulatory T cell subsets in vivo may herald their use as immunosuppressive agents in adoptive cellular therapies for autoimmune pathologies.SIGNIFICANCE STATEMENTAlthough B cells are traditionally known for their role in propagating pro-inflammatory immune responses, their immunosuppressive effects have only begun to be recently appreciated. How regulatory B cells (Bregs) suppress the immune response remains to be fully understood. In this paper we show that Bregs can induce formation of conventional regulatory T cells (Tregs) as well as type 1 regulatory T cells (Tr1). When Bregs are transferred into mice with experimental autoimmune encephalomyelitis (EAE), they home to secondary lymphoid organs, leading to an expansion of Tregs and Tr1 in vivo. Tregs and Tr1 cells are also found in greater proportions in the central nervous system of mice with EAE treated with Bregs and are correlated with remission of symptoms.%U http://www.jneurosci.org/content/jneuro/early/2016/11/07/JNEUROSCI.1994-16.2016.full.pdf
      13. URL :
        http://www.jneurosci.org/content/36/50/12598
      14. Call Number :
        PKI @ user @ 12804
      15. Serial :
        19586
      1. Author :
        Peng, Yajing; Li, Mi; Clarkson, Ben D.; Pehar, Mariana; Lao, Patrick J.; Hillmer, Ansel T.; Barnhart, Todd E.; Christian, Bradley T.; Mitchell, Heather A.; Bendlin, Barbara B.; Sandor, Matyas; Puglielli, Luigi
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2014
      5. Publication :
        The Journal of Neuroscience: The Official Journal of the Society for Neuroscience
      6. Products :
      7. Volume :
        34
      8. Issue :
        20
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Acetylation; Acetyl Coenzyme A; Animals; Endoplasmic Reticulum; G4 Pet; Infection; Inflammation; Mice; Mice, Transgenic; Neoplasms; Nerve Degeneration; X-Ray
      12. Abstract :
        The import of acetyl-CoA into the ER lumen by AT-1/SLC33A1 is essential for the N(ε)-lysine acetylation of ER-resident and ER-transiting proteins. A point-mutation (S113R) in AT-1 has been associated with a familial form of spastic paraplegia. Here, we report that AT-1S113R is unable to form homodimers in the ER membrane and is devoid of acetyl-CoA transport activity. The reduced influx of acetyl-CoA into the ER lumen results in reduced acetylation of ER proteins and an aberrant form of autophagy. Mice homozygous for the mutation display early developmental arrest. In contrast, heterozygous animals develop to full term, but display neurodegeneration and propensity to infections, inflammation, and cancer. The immune and cancer phenotypes are contingent on the presence of pathogens in the colony, whereas the nervous system phenotype is not. In conclusion, our results reveal a previously unknown aspect of acetyl-CoA metabolism that affects the immune and nervous systems and the risk for malignancies.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/24828632
      14. Call Number :
        PKI @ user @
      15. Serial :
        11782
      1. Author :
        Farrell, Helen E.; Bruce, Kimberley; Lawler, Clara; Cardin, Rhonda D.; Davis-Poynter, Nicholas J.; Stevenson, Philip G.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2016
      5. Publication :
        PLOS Pathogens
      6. Products :
      7. Volume :
        12
      8. Issue :
        12
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS; IVIS BLI in vivo
      12. Abstract :
        Cytomegaloviruses (CMVs) establish chronic, systemic infections. Peripheral infection spreads via lymph nodes, which are also a focus of host defence. Thus, this is a point at which systemic infection spread might be restricted. Subcapsular sinus macrophages (SSM) captured murine CMV (MCMV) from the afferent lymph and poorly supported its replication. Blocking the type I interferon (IFN-I) receptor (IFNAR) increased MCMV infection of SSM and of the fibroblastic reticular cells (FRC) lining the subcapsular sinus, and accelerated viral spread to the spleen. Little splenic virus derived from SSM, arguing that they mainly induce an anti-viral state in the otherwise susceptible FRC. NK cells also limited infection, killing infected FRC and causing tissue damage. They acted independently of IFNI, as IFNAR blockade increased NK cell recruitment, and NK cell depletion increased infection in IFNAR-blocked mice. Thus SSM restricted MCMV infection primarily though IFN-I, with NK cells providing a second line of defence. The capacity of innate immunity to restrict MCMV escape from the subcapsular sinus suggested that enhancing its recruitment might improve infection control.
      13. URL :
        https://doi.org/10.1371/journal.ppat.1006069 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5142805/pdf/ppat.1006069.pdf
      14. Call Number :
        PKI @ user @ 13030
      15. Serial :
        19965
      1. Author :
        Sercundes, Michelle K.; Ortolan, Luana S.; Debone, Daniela; Soeiro-Pereira, Paulo V.; Gomes, Eliane; Aitken, Elizabeth H.; Neto, Antonio Condino; Russo, Momtchilo; D' Império Lima, Maria R.; Alvarez, José M.; Portugal, Silvia; Marinho, Claudio R. F.; Epiphanio, Sabrina
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2016
      5. Publication :
        PLOS Pathogens
      6. Products :
      7. Volume :
        12
      8. Issue :
        12
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS; IVIS BLI in vivo
      12. Abstract :
        Author Summary A deeper understanding of the pathogenesis of malaria-associated ALI/ARDS may help in the development of new therapeutic approaches to improve the prognosis of severe cases of malaria. Using the Plasmodium berghei ANKA-infection mouse model of ALI/ARDS, which resembles the human disease in many aspects, this study reports the critical role of neutrophils in the pathogenesis of this syndrome. Mice developing ALI/ARDS showed abundant lung-infiltrating neutrophils in association with the increased production of neutrophil-attracting chemokines, myeloperoxidase and reactive oxygen species. The parasites Plasmodium falciparum and P. berghei ANKA both induced the formation of neutrophil extracellular traps ex vivo. By targeting neutrophils and neutrophil extracellular traps with specific drugs, we succeeded in preventing the development of malaria-associated ALI/ARDS and significantly increased mouse survival.
      13. URL :
        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5142790/pdf/ppat.1006054.pdf
      14. Call Number :
        PKI @ user @ 13044
      15. Serial :
        19511
      1. Author :
        Hartley, Mary-Anne; Bourreau, Eliane; Rossi, Matteo; Castiglioni, Patrik; Eren, Remzi Onur; Prevel, Florence; Couppié, Pierre; Hickerson, Suzanne M.; Launois, Pascal; Beverley, Stephen M.; Ronet, Catherine; Fasel, Nicolas
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2016
      5. Publication :
        PLOS Pathogens
      6. Products :
      7. Volume :
        12
      8. Issue :
        9
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS BLI; IVIS BLI in vivo
      12. Abstract :
        Author Summary Cutaneous leishmaniasis is a neglected parasitic disease particularly problematic in the South American tropics, where the parasites have an ability to migrate from the initial inoculation site in a process called “infectious metastasis”. Despite existing for centuries, the factors involved in parasite dissemination are largely unknown. We recently described that Leishmaniavirus (LRV), a virus present within some Leishmania parasites, is responsible for an exacerbation of the disease outcome in mice together with treatment failure and symptomatic relapse in human patients. In this paper we show that the expression of the pro-inflammatory cytokine IL-17A is correlated with disease chronicity in patients infected by LRV+ Leishmania parasites. We confirmed this finding in a unique murine model where IL-17A was also found to play a role in LRV1-dependent infectious metastasis. Additionally, using IL-17A as a prophylactic target, we were able to inhibit parasite proliferation and the development of infectious metastasis. Thus, we identify a pathogenic role for IL-17A in LRV1-dependent cutaneous leishmaniasis and infectious metastasis. More importantly, our data suggests that in addition to LRV presence, IL-17A is a marker of disease severity and could be a novel target to promote lesion resolution and prevent parasite dissemination.
      13. URL :
        http://dx.doi.org/10.1371%2Fjournal.ppat.1005852 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5033371/pdf/ppat.1005852.pdf
      14. Call Number :
        PKI @ user @ 12522
      15. Serial :
        19902
      1. Author :
        Bender, Ruben R.; Muth, Anke; Schneider, Irene C.; Friedel, Thorsten; Hartmann, Jessica; Plückthun, Andreas; Maisner, Andrea; Buchholz, Christian J.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2016
      5. Publication :
        PLoS Pathog
      6. Products :
      7. Volume :
        12
      8. Issue :
        6
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS; IVIS chemoluminescence
      12. Abstract :
        <title>Author Summary</title> <p>Pseudotyping of lentiviral vectors (LVs) with glycoproteins from other enveloped viruses has not only often been revealing in mechanistic studies of particle assembly and entry, but is also of practical importance for gene delivery. LVs pseudotyped with engineered glycoproteins allowing free choice of receptor usage are expected to overcome current limitations in cell-type selectivity of gene transfer. Here we describe for the first time receptor-targeted Nipah virus glycoproteins as important step towards this goal. LV particles carrying the engineered Nipah virus glycoproteins were substantially more efficient in gene delivery than their state-of-the-art measles virus-based counterparts, now making the production of receptor-targeted LVs for clinical applications possible. Moreover, the data define for the first time the molecular requirements for membrane fusion with respect to the position of the receptor binding site relative to the cell membrane, a finding with implications for the molecular evolution of paramyxoviruses using proteinaceous receptors for cell entry.</p>
      13. URL :
        http://dx.doi.org/10.1371%2Fjournal.ppat.1005641
      14. Call Number :
        PKI @ user @ 11783
      15. Serial :
        20121
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