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    题名 作者 年代 出处 被引量
1WJSC 6^(th) Anniversary Special Issues(1):Hematopoietic stem cell transplantation Allogeneic hematopoietic cell transplant for acute myeloid leukemia:Current state in 2013 and future directions显示文摘Acute myeloid leukemia(AML)represents a heterogeneous group of high-grade myeloid neoplasms of the elderly with variable outcomes.Though remissioninduction is an important first step in the management of AML,additional treatment strategies are essential to ensure long-term disease-free survival.Recent pivotal advances in understanding the genetics and molecular biology of AML have allowed for a risk-adapted approach in its management based on relapse-risk.Allogeneic hematopoietic cell transplantation(allo-HCT)represents an effective therapeutic strategy in AML providing the possibility of cure with potent graft-versus-leukemia reactions,with a demonstrable survival advantage in younger patients with intermediate-or poor-risk cytogenetics.Herein we review the published data regarding the role of allo-HCT in adults with AML.We searched MEDLINE/PubMed and EMBASE/Ovid.In addition,we searched reference lists of relevant articles,conference proceedings and ongoing trial databases.We discuss the role of allo-HCT in AML patients stratified by cytogenetic-and molecular-risk in first complete remission,as well as allo-HCT as an option in relapsed/refractory AML.Besides the conventional sibling and unrelated donor allografts,we review the available data and recent advances for alternative donor sources such as haploidentical grafts and umbilical cord blood.We also discuss conditioning regimens,including reduced intensity conditioning which has broadened the applicability of allo-HCT.Finally we explore recent advances and future possibilities and directions of allo-HCT in AML.Practical therapeutic recommendations have been made where possible based on available data and expert opinion.Abraham S Kanate Marcelo C Pasquini Parameswaran N Hari Mehdi Hamadani 2014World Journal of Stem Cells2014,6,2:6
2Microglia depletion as a therapeutic strategy:friend or foe in multiple sclerosis models?显示文摘M ultiple sclerosis is a chro nic central nervous system demyelinating disease whose onset and progression are driven by a combination of immune dysregulation,genetic predisposition,and environmental fa ctors.The activation of microglia and astrocytes is a key player in multiple sclerosis immunopathology,playing specific roles associated with anatomical location and phase of the disease and controlling demyelination and neurodegeneration.Even though reactive mic roglia can damage tissue and heighten deleterious effects and neurodegeneration,activated microglia also perform neuroprotective functions such as debris phagocytosis and growth fa ctor secretion.Astrocytes can be activated into pro-inflammato ry phenotype A1 through a mechanism mediated by activated neuroinflammatory microglia,which could also mediate neurodegeneration.This A1 phenotype inhibits oligodendrocyte prolife ration and differe ntiation and is toxic to both oligodendrocytes and neurons.Howeve r,astroglial activation into phenotype A2 may also take place in response to neurodegeneration and as a protective mechanism.A variety of animal models mimicking specific multiple sclerosis features and the associated pathophysiological processes have helped establish the cascades of events that lead to the initiation,progression,and resolution of the disease.The colonystimulating facto r-1 receptor is expressed by myeloid lineage cells such as peripheral monocytes and macrophages and central nervous system microglia.Importantly,as microglia development and survival critically rely on colony-stimulating factor-1 receptor signaling,colony-stimulating factor-1 receptor inhibition can almost completely eliminate microglia from the brain.In this context,the present review discusses the impact of microglial depletion through colo ny-stimulating factor-1 receptor inhibition on demyelination,neurodegeneration,astroglial activation,and behavior in different multiple sclerosis models,highlighting the diversity of microglial effects on the progression of demyelinating diseases and the strengths and weaknesses of microglial modulation in therapy design.Victoria Sofia Berenice Wies Mancini Anabella Ayelen Di Pietro Laura Andrea Pasquini 2023Neural Regeneration Research2023,18,2:4
3Mucosal Schwann cell “Hamartoma”:A new entity?显示文摘Schwannoma is a well-described,benign nerve sheath tumor of the soft tissue,but is rare in the gastrointestinal tract.Gastrointestinal schwannomas are often incidentally discovered as small polypoid intraluminal lesions.In this report,we describe the clinicopathologic and immunohistochemical features of a distinctive neural mucosal polyp composed of a diffuse cellular proliferation of uniform bland spindled cells in the lamina propria that entraps the colonic crypts.Immunohistochemical analysis revealed strong and diffuse positivity for the S-100 protein.To avoid confusion of these solitary colorectal polyps containing pure spindled Schwann cell proliferation in the lamina propria with neural lesions that have significant association with inherited syndromes,it is better to use the designation 'mucosal Schwann hamartoma'.Paola Pasquini Andrea Baiocchini Laura Falasca Dante Annibali Guido Gimbo Francesco Pace Franca Del Nonno 2009World Journal of Gastroenterology2009,15,18:2
4T-wave inversion after a severe head injury without ischemic heart disease显示文摘Roberto La Rocca Valeria Materia Annalisa Pasquini Felice Carmelo La Rosa Filippo Marte Salvatore Patanè 2009International Journal of Cardiology2009,,2:2
5Influence of cooking conditions on cooking loss and tenderness of raw and marinated chicken breast meat显示文摘BARBANTI D PASQUINI M 2005LWT2005,38,:1
6Evaluation of composted green waste in ornamental container-grown plants: effects on growth and plant water relations 显示文摘MUGNAI S PASQUINI T AZZARELLO E 2007Compost Science & Utilization2007,15,4:1
7Identification of counterfeit drugs using near- infrared spectroscopy显示文摘Scafi SHF Pasquini C 2001Analyst2001,126,:1
8Laser induced breakdown spectroscopy显示文摘Pasquini C Covtez J Silva L M C 2007J Braz Chem Soc2007,18,3:1
9Prime-boost vaccines encoding an intracellular idiotype/GM-CSF fusion protein induce protective cell-mediated immunity in murine pre-B cell leukemia显示文摘Pasquini S Peralta S Missiaglia E 0,,08:1
10Slructural Response of Grid-Reinforced Bituminous Pavement显示文摘Andrea Graziani Emiliano Pasquini Gilda Ferrolti 2014Materials and Struclures2014,47,8:1
11Endoscopic treatment of benign tumors of the nose and paranasal sunuses: a report of 33 cases显示文摘SCIARRETTA V PASQUINI E FRANK G 2006Am J Rhinol2006,20,1:1
12Total anomalous pulmonary venous connection:Long-term appraisal with evolving technical solutions显示文摘Michielon G DiDonato RM Pasquini L 2002Eur J Cardiothorac Surg2002,22,2:1
13A small molecule SMAC mimic LBW242 potentiates TRAIL-and anticancer drug-mediated cell death of ovarian cancer cells显示文摘Petrucci E Pasquini L Bernabei M 0,,:1
14Gemcitabine in advanced NSCLC of elderly:A phase Ⅱ study显示文摘 Tassinari D Niconlini M 1998Ann Oncol1998,,:1
15The Effects of Fetal Blood Sampling on Ventricular Filling Patterns: Differences Between Normally Grown and Growth-Retarded Fetuses显示文摘Alessandra Capponi Giuseppe Rizzo Luciano Pasquini Domenico Arduini Carolo Romanini 1996Amer J Perinatol1996,,08:1
16What Determines University Pa- tent Commercialization? Empirical Evidence on the Role of Uni- versity IPR Ownership 显示文摘Giuri P Munad F Pasquini M 2013Industry and Innovation2013,20,5:1
17Motor and functional recovery in patients with poet-stroke,depression显示文摘Nannetti L paci M pasquini J 2005Disabil rehabil2005,27,4:1
18Total anomalous pulmonary venous connection:long-term appraisal with evolving technical solutions显示文摘Michielon G Di Donato RM Pasquini L 2002Eur J Cardiothorac Surg2002,22,2:1
19Nilotinib ver- sus imatinib in patients (pts) with newly diagnosed philadelphia chromosome-positive ( Ph + ) chronic myeloid leukemla in ehron- ic phase (CML-CP) : ENESTnd 36-month (too) follow-up显示文摘SAGLIO G LECOUTRE PD PASQUINI R 2011Blood2011,118,:1
20Cuprizone-induced de- myelination in the rat cerebral cortex and thyroid hormore effects on cortical remyelination 显示文摘Silvestroff L Bartucci S Pasquini J 2012Exp Neurol2012,235,1:1
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