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Search Results: 1 - 10 of 297496 matches for " J. Diefenbach "
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Emerging role of carfilzomib in treatment of relapsed and refractory lymphoid neoplasms and multiple myeloma
Jain S, Diefenbach C, Zain J, O'Connor OA
Core Evidence , 2011, DOI: http://dx.doi.org/10.2147/CE.S13838
Abstract: ging role of carfilzomib in treatment of relapsed and refractory lymphoid neoplasms and multiple myeloma Review (6247) Total Article Views Authors: Jain S, Diefenbach C, Zain J, O'Connor OA Published Date April 2011 Volume 2011:6 Pages 43 - 57 DOI: http://dx.doi.org/10.2147/CE.S13838 Salvia Jain, Catherine Diefenbach, Jasmine Zain, Owen A O’Connor NYU Cancer Institute, Division of Hematology and Medical Oncology, NYU Langone Medical Center, New York, NY, USA Abstract: Proteasome inhibition forms the cornerstone of antimyeloma therapy. The first-in-class proteasome inhibitor, bortezomib, either alone or in combination with other chemotherapeutic agents, induces high overall response rates and response qualities in patients with clinically and molecularly defined high-risk disease. However, resistance to bortezomib and neurotoxicity associated with the treatment remain challenging issues. Carfilzomib is a novel, well tolerated, irreversible proteasome inhibitor with minimal neurotoxicity. Carfilzomib demonstrates promising activity in myeloma patients who are refractory to bortezomib and immunomodulatory agents. This review focuses on the pharmacology, safety, and efficacy of carfilzomib for the treatment of multiple myeloma in bortezomib-na ve and bortezomib-exposed populations.
Emerging role of carfilzomib in treatment of relapsed and refractory lymphoid neoplasms and multiple myeloma
Jain S,Diefenbach C,Zain J,O'Connor OA
Core Evidence , 2011,
Abstract: Salvia Jain, Catherine Diefenbach, Jasmine Zain, Owen A O’ConnorNYU Cancer Institute, Division of Hematology and Medical Oncology, NYU Langone Medical Center, New York, NY, USAAbstract: Proteasome inhibition forms the cornerstone of antimyeloma therapy. The first-in-class proteasome inhibitor, bortezomib, either alone or in combination with other chemotherapeutic agents, induces high overall response rates and response qualities in patients with clinically and molecularly defined high-risk disease. However, resistance to bortezomib and neurotoxicity associated with the treatment remain challenging issues. Carfilzomib is a novel, well tolerated, irreversible proteasome inhibitor with minimal neurotoxicity. Carfilzomib demonstrates promising activity in myeloma patients who are refractory to bortezomib and immunomodulatory agents. This review focuses on the pharmacology, safety, and efficacy of carfilzomib for the treatment of multiple myeloma in bortezomib-na ve and bortezomib-exposed populations.Keywords: carfilzomib, multiple myeloma, pharmacology, safety, efficacy
Role of the Aryl Hydrocarbon Receptor in Controlling Maintenance and Functional Programs of RORγt+ Innate Lymphoid Cells and Intraepithelial Lymphocytes
Andreas Diefenbach
Frontiers in Immunology , 2012, DOI: 10.3389/fimmu.2012.00124
Abstract: Mucosal retinoic receptor-related orphan receptor (ROR)γt-expressing innate lymphoid cells (ILC) play an important role in the defense against intestinal pathogens and in promoting epithelial homeostasis and adaptation, thereby effectively protecting the vertebrate host against intestinal inflammatory disorders. The functional activity of RORγt+ ILC is under the control of environmental cues. However, the molecular sensors for such environmental signals are largely unknown. Recently, the aryl hydrocarbon receptor (AhR) has emerged as a master regulator for the postnatal maintenance of intestinal RORγt+ ILC and intraepithelial lymphocytes. AhR is a highly conserved transcription factor whose activity is regulated by environmental and dietary small molecule ligands. Here, we review the role of AhR signaling for the maintenance of intestinal immune cells and its impact on the immunological protection against intestinal infections and debilitating chronic inflammatory disorders.
Annual survival estimation of migratory songbirds confounded by incomplete breeding site-fidelity: study designs that may help
Marshall, M. R.,Diefenbach, D. R.,Wood, L. A.,Cooper, R. J.
Animal Biodiversity and Conservation , 2004,
Abstract: Many species of bird exhibit varying degrees of site-fidelity to the previous year's territory or breeding area, a phenomenon we refer to as incomplete breeding site-fidelity. If the territory they occupy is located beyond the bounds of the study area or search area (i.e., they have emigrated from the study area), the bird will go undetected and is therefore indistinguishable from dead individuals in capture-mark-recapture studies. Differential emigration rates confound inferences regarding differences in survival between sexes and among species if apparent survival rates are used as estimates of true survival. Moreover, the bias introduced by using apparent survival rates for true survival rates can have profound effects on the predictions of population persistence through time, source/sink dynamics, and other aspects of life-history theory. We investigated four study design and analysis approaches that result in apparent survival estimates that are closer to true survival estimates. Our motivation for this research stemmed from a multi-year capture-recapture study of Prothonotary Warblers (Protonotaria citrea) on multiple study plots within a larger landscape of suitable breeding habitat where substantial inter-annual movements of marked individuals among neighboring study plots was documented. We wished to quantify the effects of this type of movement on annual survival estimation. The first two study designs we investigated involved marking birds in a core area and resighting them in the core as well as an area surrounding the core. For the first of these two designs, we demonstrated that as the resighting area surrounding the core gets progressively larger, and more 'emigrants' are resighted, apparent survival estimates begin to approximate true survival rates (bias < 0.01). However, given observed inter-annual movements of birds, it is likely to be logistically impractical to resight birds on sufficiently large surrounding areas to minimize bias. Therefore, as an alternative protocol, we analyzed the data with subsets of three progressively larger areas surrounding the core. The data subsets provided four estimates of apparent survival that asymptotically approached true survival. This study design and analytical approach is likely to be logistically feasible in field settings and yields estimates of true survival unbiased (bias < 0.03) by incomplete breeding site-fidelity over a range of inter annual territory movement patterns. The third approach we investigated used a robust design data collection and analysis approach. This approach resulted i
Habitat Availability Is a More Plausible Explanation than Insecticide Acute Toxicity for U.S. Grassland Bird Species Declines
Jason M. Hill, J. Franklin Egan, Glenn E. Stauffer, Duane R. Diefenbach
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0098064
Abstract: Grassland bird species have experienced substantial declines in North America. These declines have been largely attributed to habitat loss and degradation, especially from agricultural practices and intensification (the habitat-availability hypothesis). A recent analysis of North American Breeding Bird Survey (BBS) “grassland breeding” bird trends reported the surprising conclusion that insecticide acute toxicity was a better correlate of grassland bird declines in North America from 1980–2003 (the insecticide-acute-toxicity hypothesis) than was habitat loss through agricultural intensification. In this paper we reached the opposite conclusion. We used an alternative statistical approach with additional habitat covariates to analyze the same grassland bird trends over the same time frame. Grassland bird trends were positively associated with increases in area of Conservation Reserve Program (CRP) lands and cropland used as pasture, whereas the effect of insecticide acute toxicity on bird trends was uncertain. Our models suggested that acute insecticide risk potentially has a detrimental effect on grassland bird trends, but models representing the habitat-availability hypothesis were 1.3–21.0 times better supported than models representing the insecticide-acute-toxicity hypothesis. Based on point estimates of effect sizes, CRP area and agricultural intensification had approximately 3.6 and 1.6 times more effect on grassland bird trends than lethal insecticide risk, respectively. Our findings suggest that preserving remaining grasslands is crucial to conserving grassland bird populations. The amount of grassland that has been lost in North America since 1980 is well documented, continuing, and staggering whereas insecticide use greatly declined prior to the 1990s. Grassland birds will likely benefit from the de-intensification of agricultural practices and the interspersion of pastures, Conservation Reserve Program lands, rangelands and other grassland habitats into existing agricultural landscapes.
Polarization dependent, surface plasmon induced photoconductance in gold nanorod arrays
S. Diefenbach,N. Erhard,J. Schopka,A. Martin,C. Karnetzky,D. Iacopino,A. W. Holleitner
Physics , 2013, DOI: 10.1002/pssr.201308305
Abstract: We report on the photoconductance in two-dimensional arrays of gold nanorods which is strongly enhanced at the frequency of the longitudinal surface plasmon of the nanorods. The arrays are formed by a combination of droplet deposition and stamping of gold nanorod solutions on SiO2 substrates. We find that the plasmon induced photoconductance is sensitive to the linear polarization of the exciting photons. We interpret the occurrence of the photoconductance as a bolometric enhancement of the arrays' conductance upon excitation of the longitudinal surface plasmon resonance of the nanorods.
Muscle Invasive Bladder Cancer: From Diagnosis to Survivorship
N. E. Mohamed,M. A. Diefenbach,H. H. Goltz,C. T. Lee,D. Latini,M. Kowalkowski,C. Philips,W. Hassan,S. J. Hall
Advances in Urology , 2012, DOI: 10.1155/2012/142135
Abstract: Bladder cancer is the fifth most commonly diagnosed cancer and the most expensive adult cancer in average healthcare costs incurred per patient in the USA. However, little is known about factors influencing patients' treatment decisions, quality of life, and responses to treatment impairments. The main focus of this paper is to better understand the impact of muscle invasive bladder cancer on patient quality of life and its added implications for primary caregivers and healthcare providers. In this paper, we discuss treatment options, side effects, and challenges that patients and family caregivers face in different phases along the disease trajectory and further identify crucial areas of needed research. 1. Introduction Cancer diagnosis is often perceived as a traumatic event that changes an individual’s basic assumptions about the self as effective and powerful, and the world as benevolent, controllable, and predictable [1, 2]. This event is even more devastating when cancer patients undergo extensive surgeries that severely debilitate their body image and their psychological and social well-being. Muscle-invasive bladder cancer (MIBC) provides a powerful, yet understudied example of the impact that cancer diagnosis and treatments may have on patients’ emotional, physical, functional, and social adjustment [3]. Previous research in this patient population has primarily been focused on health-related quality of life (HRQOL) as an indicator of posttreatment adjustment [4]. Yet, in addition to decrements in HRQOL and body image, patients with MIBC must often resolve treatment decision-related conflicts and overcome financial, communication, literacy, and healthcare service barriers as they move through different phases of the cancer trajectory (i.e., cancer diagnosis, treatment, and survivorship). Despite treatment-related physical and social limitations, patients need to: (1) balance the uncertainty associated with diagnosis and the risk of recurrence; (2) maintain previous social roles and functions; (3) solve financial issues arising from insurance issues and uncertain employment situations. In this paper, we will provide a comprehensive overview of: (1) MIBC incidence, mortality rates, and risk factors; (2) MIBC-treatment-related side effects; (3) challenges that newly diagnosed MIBC patients face during treatment decision making, treatment-related side effects, and posttreatment healthcare; (4) indicators of posttreatment adjustment survivorship issues. We will address limitations in the existing literature and discuss future directions. 2. Radical
Novel Approaches to Detect Serum Biomarkers for Clinical Response to Interferon-β Treatment in Multiple Sclerosis
Kaushal S. Gandhi,Fiona C. McKay,Eve Diefenbach,Ben Crossett,Stephen D. Schibeci,Robert N. Heard,Graeme J. Stewart,David R. Booth,Jonathan W. Arthur
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0010484
Abstract: Interferon beta (IFNβ) is the most common immunomodulatory treatment for relapsing-remitting multiple sclerosis (RRMS). However, some patients fail to respond to treatment. In this study, we identified putative clinical response markers in the serum and plasma of people with multiple sclerosis (MS) treated with IFNβ. In a discovery-driven approach, we use 2D-difference gel electrophoresis (DIGE) to identify putative clinical response markers and apply power calculations to identify the sample size required to further validate those markers. In the process we have optimized a DIGE protocol for plasma to obtain cost effective and high resolution gels for effective spot comparison. APOA1, A2M, and FIBB were identified as putative clinical response markers. Power calculations showed that the current DIGE experiment requires a minimum of 10 samples from each group to be confident of 1.5 fold difference at the p<0.05 significance level. In a complementary targeted approach, Cytometric Beadarray (CBA) analysis showed no significant difference in the serum concentration of IL-6, IL-8, MIG, Eotaxin, IP-10, MCP-1, and MIP-1α, between clinical responders and non-responders, despite the association of these proteins with IFNβ treatment in MS.
First evidence of overlaps between HIV-Associated Dementia (HAD) and non-viral neurodegenerative diseases: proteomic analysis of the frontal cortex from HIV+ patients with and without dementia
Li Zhou, Eve Diefenbach, Ben Crossett, Sieu L Tran, Thomas Ng, Helen Rizos, Rejane Rua, Bin Wang, Amit Kapur, Kaushal Gandhi, Bruce J Brew, Nitin K Saksena
Molecular Neurodegeneration , 2010, DOI: 10.1186/1750-1326-5-27
Abstract: Here, we have analyzed total proteins from the frontal cortex of 9 HAD and 5 HIV non-dementia patients. Using 2-Dimensional differential in-gel electrophoresis (2-DIGE) to analyze the brain tissue proteome, 76 differentially expressed proteins (p < 0.05; fold change>1.25) were identified between HAD and HIV non-dementia patients, of which 36 protein spots (based on 3D appearance of spots on the images) were chosen for the mass spectrometry analysis. The large majority of identified proteins were represented in the energy metabolic (mitochondria) and signal transduction pathways. Furthermore, over 90% of the protein candidates are common to both HAD and other non-viral neurodegenerative disease, such as Alzheimer's disease. The data was further validated using specific antibodies to 4 proteins (CA2, GS, CKMT and CRMP2) by western blot (WB) in the same samples used for 2D-DIGE, with additional confirmation by immunohistochemitsry (IHC) using frontal lobe tissue from different HAD and HIV+ non-dementia patients. The validation for all 4 antibodies by WB and IHC was in concordance with the DIGE results, lending further credence to the current findings.These results suggest not only convergent pathogenetic pathways for the two diseases but also the possibility of increased Alzheimer's disease (AD) susceptibility in HAD patients whose life expectancy has been significantly increased by highly active antiretroviral therapy.HIV-1 associated dementia (HAD) is a common complication of HIV disease with a prevalence of at least 20% in advanced HIV infection in the pre-highly active antiretroviral therapy (HAART) era [1]. Even in patients taking HAART, milder forms of cognitive impairment remain common and functionally significant [2]. The reasons for the continued presence and development of HAD and its milder forms, despite effective HAART are not clear. Furthermore, due to the longevity of HIV patients after the advent of HAART, the prevalence of HAD has increased [3]. It has
A36-dependent Actin Filament Nucleation Promotes Release of Vaccinia Virus
Jacquelyn Horsington,Helena Lynn,Lynne Turnbull,Delfine Cheng,Filip Braet,Russell J. Diefenbach,Cynthia B. Whitchurch,Guna Karupiah,Timothy P. Newsome
PLOS Pathogens , 2013, DOI: 10.1371/journal.ppat.1003239
Abstract: Cell-to-cell transmission of vaccinia virus can be mediated by enveloped virions that remain attached to the outer surface of the cell or those released into the medium. During egress, the outer membrane of the double-enveloped virus fuses with the plasma membrane leaving extracellular virus attached to the cell surface via viral envelope proteins. Here we report that F-actin nucleation by the viral protein A36 promotes the disengagement of virus attachment and release of enveloped virus. Cells infected with the A36YdF virus, which has mutations at two critical tyrosine residues abrogating localised actin nucleation, displayed a 10-fold reduction in virus release. We examined A36YdF infected cells by transmission electron microscopy and observed that during release, virus appeared trapped in small invaginations at the plasma membrane. To further characterise the mechanism by which actin nucleation drives the dissociation of enveloped virus from the cell surface, we examined recombinant viruses by super-resolution microscopy. Fluorescently-tagged A36 was visualised at sub-viral resolution to image cell-virus attachment in mutant and parental backgrounds. We confirmed that A36YdF extracellular virus remained closely associated to the plasma membrane in small membrane pits. Virus-induced actin nucleation reduced the extent of association, thereby promoting the untethering of virus from the cell surface. Virus release can be enhanced via a point mutation in the luminal region of B5 (P189S), another virus envelope protein. We found that the B5P189S mutation led to reduced contact between extracellular virus and the host membrane during release, even in the absence of virus-induced actin nucleation. Our results posit that during release virus is tightly tethered to the host cell through interactions mediated by viral envelope proteins. Untethering of virus into the surrounding extracellular space requires these interactions be relieved, either through the force of actin nucleation or by mutations in luminal proteins that weaken these interactions.
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