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| 1 | Brain stem cells as the cell of origin in glioma显示文摘Glioma incidence rates in the United States are near 20000 new cases per year, with a median survival time of 14.6 mo for high-grade gliomas due to limited therapeutic options. The origins of these tumors and their many subtypes remain a matter of investigation. Evidence from mouse models of glioma and human clinical data have provided clues about the cell types and initiating oncogenic mutations that drive gliomagenesis, a topic we review here. There has been mixed evidence as to whether or not the cells of origin are neural stem cells, progenitor cells or differentiated progeny. Many of the existing murine models target cell populations defined by lineage-specific promoters or employ lineagetracing methods to track the potential cells of origin. Our ability to target specific cell populations will likely increase concurrently with the knowledge gleaned from an understanding of neurogenesis in the adult brain. The cell of origin is one variable in tumorigenesis, as oncogenes or tumor suppressor genes may differentially transform the neuroglial cell types. Knowledge of key driver mutations and susceptible cell types will allow us to understand cancer biology from a developmental standpoint and enable early interventional strategies and biomarker discovery. | Aram S Modrek N Sumru Bayin Dimitris G Placantonakis | 2014 | World Journal of Stem Cells2014，6，1： | 12 |
| 2 | Selected properties of high- volume fly ash concretes 显示文摘 | Sivasund Aram V Carette G G Malhotra V M | 1990 | Concrete Inst: design con- struction1990，12，10： | 1 |
| 3 | Multimodal monitoring for hemodynamic categorization and management of pediatric septic shock显示文摘 | Ranjit S Aram G Kissoon N | 2014 | Pediatric Critical Care Medicine2014，15，1： | 1 |
| 4 | Identifying patterns and relationships among the responses of seventh-grade students to the science process skill of designing experiment显示文摘 | Germann P.J Aram R Burke G | | 0，，： | 1 |
| 5 | Adhesion control of cyclin DI and p27Kipl levels is deregulated in melanoma cells through BRAF MEK-ERKsignaling显示文摘 | Bhatt KV Spofford LS Aram G | | 0，，： | 1 |
| 6 | Metastasis of esophageal cancer to finger显示文摘 | Seyed-Reza M Afshin G Aram T | 2005 | Arch Iran Med2005，8，： | 1 |
| 7 | The hierarchy of needs theory: an evaluation in Chile 显示文摘 | Aram J D Piraino T G | 1978 | Inter - American Journal of Psychology1978，12，2： | 1 |
| 8 | Some aspects of the role of surfactants in the formation of nanoparticles 显示文摘 | Sharad G Dixit Anand R Mahadeshwar Santosh K H aram | 1998 | Colloids and Surfaces A: Physicochemical and Engineering Aspects1998，133，7： | 1 |
| 9 | Deficiency of nicotinamide adenine dinucleotide phosphate, reduced form oxidase enhances hepatocellular injury but attenuates fibrosis after chronic, carbon tetraehloride administration显示文摘 | ARAM G POTTER J J LIU X | 2009 | Hepatology2009，49，3： | 1 |
| 10 | Deficiency of nicotinamide adenine dinucleotide phosphate,reduced form oxidase enhances hepatocellular injury but attenuates fibrosis after chronic carbon tetrachloride administration显示文摘 | Aram G Potter J J Liu X | | 0，，03： | 1 |
| 11 | Purinergic receptor-medi- ated rapid depletion of nuclear phosphorylated Akt depends on pleckstrin homology domain leucine-rieh repeat phosphatase, cal- cineurin, protein phosphatase 2A, and PTEN phosphatases 显示文摘 | Mistafa O Aram G Sandeep K | 2010 | Biol Chem2010，285，27： | 1 |
| 12 | Deficiency of nicotinamide adenine dinucleotide phosphate, reduced form oxidase enhances hepatocellular injury but attenuates fibrosis after chronic carbon tetrachloride administration显示文摘 | Aram G Potter J J Liu X | 2009 | Hepatology2009，49，3： | 1 |
| 13 | Deficiency of nicotinamide adenine dinucleotide phosphate, reduced form oxidase enhanceshe hepatocellular injury but attenuates fibrosis after chronic carbon tetrachloride administration显示文摘 | Aram G Potter JJ Liu X | 2009 | Hepatology2009，49，： | 1 |
| 14 | Photoreceptor differentiation and integration of retinal progenitor cells transplanted into transgenic rats显示文摘 | Qiu G Seiler MJ Mui C Arai S Aramant RB deJuan E Jr | | 0，，04： | 1 |
| 15 | 水痘-带状疱疹病毒毛囊炎促进克隆性淋巴样增生显示文摘Post herpes zoster (HZ) reactions have been associated with panoply of neoplastic, inflammatory, and fibro-inflammatory cutaneous disorders. Varicella zoster virus (VZV) DNA has not been identified in most of these reports. After an episode of HZ, a healthy, active 90-year-old female developed ulcerative nodules in the affected trigeminal V1 dermatome and the contra-lateral trigeminal region over a 1-year period. Excision and/or biopsy of all these lesions showed similar pathologic changes that consisted of herpetic folliculitis, adjacent dense mixed nodular lymphocytic infiltrates with germinal centers (cutaneous lymphoid hyperplasia (CLH)), and in the deeper excision specimens, an obliterative vasculitis of a vessel with smooth muscle in its wall. Immunophenotype analysis revealed a mixed, predominate T-and B-cell population without loss of pan-T cell antigens or aberrant expression by B cells of T-cell antigens. Polymerase chain reaction for herpetic DNA was po sitive for VZV DNA. Lymphocyte gene rearrangement analysis revealed 2 distinct, anatomically and chronologically, monoclonal B-cell populations and a monoclona l T-cell population in one nodule. Treatment with valacyclovir has lead to almo st complete resolution of her cutaneous nodules after 6 months of therapy. In th is case, it can be surmised that persistence of VZV infection and lack of effect ive cell-mediated immunity lead to development of both immunopathology (vasculi tis) and excessive lymphoid cell proliferation (CLH). | Aram G Rohwedder A Nazeer T J.A. Carlson 党倩丽 | 2006 | 世界核心医学期刊文摘(皮肤病学分册)2006，0，1： | 0 |
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