Materials Science-medziagotyra最新文献

{"title":"WITHDRAWN: Cardio-Oncology: Stronger Together.","authors":"Richard J Kovacs, Howard A Burris","doi":"10.1016/j.jacc.2019.07.041","DOIUrl":"10.1016/j.jacc.2019.07.041","url":null,"abstract":"<p><p>This article has been removed from JACC where it was posted in error. It is an article for JACC: CardioOncology (10.1016/j.jaccao.2019.08.001) and will be included in the first issue. The full Elsevier Policy on Article Withdrawal can be found at https://www.elsevier.com/about/our-business/policies/article-withdrawal.</p>","PeriodicalId":18298,"journal":{"name":"Materials Science-medziagotyra","volume":"46 1","pages":""},"PeriodicalIF":24.0,"publicationDate":"2019-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74068787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Origin and structure of polar domains in doped molecular crystals.","authors":"E Meirzadeh, I Azuri, Y Qi, D Ehre, A M Rappe, M Lahav, L Kronik, I Lubomirsky","doi":"10.1038/ncomms13351","DOIUrl":"10.1038/ncomms13351","url":null,"abstract":"<p><p>Doping is a primary tool for the modification of the properties of materials. Occlusion of guest molecules in crystals generally reduces their symmetry by the creation of polar domains, which engender polarization and pyroelectricity in the doped crystals. Here we describe a molecular-level determination of the structure of such polar domains, as created by low dopant concentrations (<0.5%). The approach comprises crystal engineering and pyroelectric measurements, together with dispersion-corrected density functional theory and classical molecular dynamics calculations of the doped crystals, using neutron diffraction data of the host at different temperatures. This approach is illustrated using centrosymmetric α-glycine crystals doped with minute amounts of different L-amino acids. The experimentally determined pyroelectric coefficients are explained by the structure and polarization calculations, thus providing strong support for the local and global understanding of how different dopants influence the properties of molecular crystals.</p>","PeriodicalId":18298,"journal":{"name":"Materials Science-medziagotyra","volume":"56 1","pages":"13351"},"PeriodicalIF":16.6,"publicationDate":"2016-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5105173/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"58120342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Initiator Methionine tRNA Drives Secretion of Type II Collagen from Stromal Fibroblasts to Promote Tumor Growth and Angiogenesis.","authors":"Cassie J Clarke, Tracy J Berg, Joanna Birch, Darren Ennis, Louise Mitchell, Catherine Cloix, Andrew Campbell, David Sumpton, Colin Nixon, Kirsteen Campbell, Victoria L Bridgeman, Peter B Vermeulen, Shane Foo, Eleftherios Kostaras, J Louise Jones, Linda Haywood, Ellie Pulleine, Huabing Yin, Douglas Strathdee, Owen Sansom, Karen Blyth, Iain McNeish, Sara Zanivan, Andrew R Reynolds, Jim C Norman","doi":"10.1016/j.cub.2016.01.045","DOIUrl":"10.1016/j.cub.2016.01.045","url":null,"abstract":"<p><p>Expression of the initiator methionine tRNA (tRNAi(Met)) is deregulated in cancer. Despite this fact, it is not currently known how tRNAi(Met) expression levels influence tumor progression. We have found that tRNAi(Met) expression is increased in carcinoma-associated fibroblasts, implicating deregulated expression of tRNAi(Met) in the tumor stroma as a possible contributor to tumor progression. To investigate how elevated stromal tRNAi(Met) contributes to tumor progression, we generated a mouse expressing additional copies of the tRNAi(Met) gene (2+tRNAi(Met) mouse). Growth and vascularization of subcutaneous tumor allografts was enhanced in 2+tRNAi(Met) mice compared with wild-type littermate controls. Extracellular matrix (ECM) deposited by fibroblasts from 2+tRNAi(Met) mice supported enhanced endothelial cell and fibroblast migration. SILAC mass spectrometry indicated that elevated expression of tRNAi(Met) significantly increased synthesis and secretion of certain types of collagen, in particular type II collagen. Suppression of type II collagen opposed the ability of tRNAi(Met)-overexpressing fibroblasts to deposit pro-migratory ECM. We used the prolyl hydroxylase inhibitor ethyl-3,4-dihydroxybenzoate (DHB) to determine whether collagen synthesis contributes to the tRNAi(Met)-driven pro-tumorigenic stroma in vivo. DHB had no effect on the growth of syngeneic allografts in wild-type mice but opposed the ability of 2+tRNAi(Met) mice to support increased angiogenesis and tumor growth. Finally, collagen II expression predicts poor prognosis in high-grade serous ovarian carcinoma. Taken together, these data indicate that increased tRNAi(Met) levels contribute to tumor progression by enhancing the ability of stromal fibroblasts to synthesize and secrete a type II collagen-rich ECM that supports endothelial cell migration and angiogenesis.</p>","PeriodicalId":18298,"journal":{"name":"Materials Science-medziagotyra","volume":"53 1","pages":"755-65"},"PeriodicalIF":9.2,"publicationDate":"2016-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4819511/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"54073208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNA-203 suppresses gastric cancer growth by targeting PIBF1/Akt signaling.","authors":"Shao-Jun Chu, Ge Wang, Peng-Fei Zhang, Rui Zhang, Yan-Xia Huang, Yun-Min Lu, Wei Da, Qun Sun, Jing Zhang, Jin-Shui Zhu","doi":"10.1186/s13046-016-0323-1","DOIUrl":"10.1186/s13046-016-0323-1","url":null,"abstract":"<p><strong>Background: </strong>MicroRNAs (miRNAs) have been proved involved in many tumorigenic behaviors including tumor growth. But, the clinical significance and functions of miRNA-203 in gastric cancer (GC) remain elusive.</p><p><strong>Results: </strong>Decreased expression of miRNA-203 was correlated with tumor size, poor prognosis and recurrence in GC patients. Overexpression of miR-203 or knockdown of its target progesterone immunomodulatory binding factor 1 (PIBF1) inhibited GC growth in vitro and in vivo, while miR-203 knockdown promoted GC proliferation. In addition, PIBF1 overexpression attenuated the inhibitory effects of miR-203 on GC growth and enhanced that effect on p-Akt expression.</p><p><strong>Conclusions: </strong>MiR-203 as a tumor biomarker suppresses GC growth through targeting the PIBF1/Akt signaling, suggesting that it may have the important therapeutic potential for the treatment of GC.</p>","PeriodicalId":18298,"journal":{"name":"Materials Science-medziagotyra","volume":"47 1","pages":"47"},"PeriodicalIF":11.3,"publicationDate":"2016-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4791790/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74071848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of synthesis time on morphology of hollow porous silica microspheres","authors":"Qiang Chen, Juha Larismaa, Anu Keski-Honkola, K. Vilonen, O. Söderberg, S. Hannula","doi":"10.5755/J01.MS.18.1.1344","DOIUrl":"https://doi.org/10.5755/J01.MS.18.1.1344","url":null,"abstract":"Hollow porous silica microspheres may be applicable as containers for the controlled release in drug delivery systems (DDS), foods, cosmetics, agrochemical, textile industry, and in other technological encapsulation use. In order to control the surface morphological properties of the silica microspheres, the effect of synthesis time on their formation was studied by a method of water-in-oil (W/O) emulsion mediated sol-gel techniques. An aqueous phase of water, ammonium hydroxide and a surfactant Tween 20 was emulsified in an oil phase of 1-octanol with a stabilizer, hydroxypropyl cellulose (HPC), and a surfactant, sorbitan monooleate (Span 80) with low hydrophile-lipophile balance (HLB) value. Tetraethyl orthosilicate (TEOS) as a silica precursor was added to the emulsion. The resulting silica particles at different synthesis time 24, 48, and 72 hours were air-dried at room temperature and calcinated at 773 K for 3 hours. The morphology of the particles was characterized by scanning electron microscopy and the particle size distribution was measured by laser diffraction. The specific surface areas were studied by 1-point BET method, and pore sizes were measured by Image Tool Software. Both dense and porous silica microspheres were observed after all three syntheses. Hollow porous silica microspheres were formed at 24 and 48 hours synthesis time. Under base catalyzed sol-gel solution, the size of silica particles was in the range of 5.4 μm to 8.2 μm, and the particles had surface area of 111 m 2 /g – 380 m 2 /g. The longer synthesis time produced denser silica spheres with decreased pore sizes. DOI: http://dx.doi.org/10.5755/j01.ms.18.1.1344","PeriodicalId":18298,"journal":{"name":"Materials Science-medziagotyra","volume":"27 1","pages":"66-71"},"PeriodicalIF":1.0,"publicationDate":"2012-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76702533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A dominant negative mutant of the KCC1 K-Cl cotransporter: both N- and C-terminal cytoplasmic domains are required for K-Cl cotransport activity.","authors":"S Casula, B E Shmukler, S Wilhelm, A K Stuart-Tilley, W Su, M N Chernova, C Brugnara, S L Alper","doi":"10.1074/jbc.M107155200","DOIUrl":"10.1074/jbc.M107155200","url":null,"abstract":"<p><p>K-Cl cotransport regulates cell volume and chloride equilibrium potential. Inhibition of erythroid K-Cl cotransport has emerged as an important adjunct strategy for the treatment of sickle cell anemia. However, structure-function relationships among the polypeptide products of the four K-Cl cotransporter (KCC) genes are little understood. We have investigated the importance of the N- and C-terminal cytoplasmic domains of mouse KCC1 to its K-Cl cotransport function expressed in Xenopus oocytes. Truncation of as few as eight C-terminal amino acids (aa) abolished function despite continued polypeptide accumulation and surface expression. These C-terminal loss-of-function mutants lacked a dominant negative phenotype. Truncation of the N-terminal 46 aa diminished function. Removal of 89 or 117 aa (Delta(N)117) abolished function despite continued polypeptide accumulation and surface expression and exhibited dominant negative phenotypes that required the presence of the C-terminal cytoplasmic domain. The dominant negative loss-of-function mutant Delta(N)117 was co-immunoprecipitated with wild type KCC1 polypeptide, and its co-expression did not reduce wild type KCC1 at the oocyte surface. Delta(N)117 also exhibited dominant negative inhibition of human KCC1 and KCC3 and, with lower potency, mouse KCC4 and rat KCC2.</p>","PeriodicalId":18298,"journal":{"name":"Materials Science-medziagotyra","volume":"54 1","pages":"41870-8"},"PeriodicalIF":0.0,"publicationDate":"2001-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1074/jbc.M107155200","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85645168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}