5 results on '"Aaron C. Zhang"'
Search Results
2. Incidence and mortality trends of metastatic prostate cancer: Surveillance, Epidemiology, and End Results database analysis
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Aaron C. Zhang, Anne Golden, Rehana Rasul, and Michael A. Feuerstein
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Oncology ,medicine.medical_specialty ,business.industry ,Proportional hazards model ,Urology ,Incidence (epidemiology) ,Rate ratio ,medicine.disease ,Prostate cancer ,Prostate cancer screening ,medicine.anatomical_structure ,Prostate ,Internal medicine ,Epidemiology ,medicine ,Surveillance, Epidemiology, and End Results ,business ,Original Research - Abstract
Introduction: In the past decade, prostate cancer screening decreased, raising the concern of delays in diagnosis and leading to increase in new cases of metastatic prostate cancer. This study evaluated whether these changes may have impacted trends in metastatic prostate cancer incidence and survival. Methods: Metastatic prostate cancer diagnoses from 2008–2016 were identified from the Surveillance, Epidemiology, and End Results (SEER) 18 registries. Age-adjusted incidence rates per 100 000 were calculated by time periods and demographic variables. Two-year all-cause and prostate cancer-specific mortality were calculated for patients diagnosed from 2008–2014, and multivariable Cox proportional hazards models were used to evaluate the impact of demographic and clinical variables. Results: Incidence rates of metastatic prostate cancer increased by 18% from 2008–2009 to 2014–2016 (Incidence rate ratio [IRR]=1.18, 95% confidence interval [CI] 1.14–1.21). This trend was observed across multiple subgroups but was greatest in non-Hispanic Whites and patients living in counties 0–10% below poverty level. There was an overall decreased risk of all-cause and prostate cancer-specific mortality, but unmarried men and men living in counties >20% below poverty level showed statistically significant increased risk of prostate cancer-specific mortality. Conclusions: Non-Hispanic Whites and the wealthiest subgroups had the largest increase in incidence of metastatic prostate cancer since 2008. Despite trends of decreased risk of prostate cancer-specific mortality, we found certain populations experienced increases in mortality risk. Studies exploring the role of socioeconomic factors on screening and access to newer treatments are needed.
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- 2021
3. Eruptions and related clinical course among 296 hospitalized adults with confirmed COVID-19
- Author
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Stephanie K. Lin, Morgan Birabaharan, Eric C. Lee, Erika Rivera, Ashna Joseph, Rachel Tannenbaum, Sergey Rekhtman, John Chelico, Andrew Strunk, Michael Qiu, Nicole Grbic, Amit Garg, Shari Wright, and Aaron C. Zhang
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Male ,Erythema ,medicine.medical_treatment ,BMI, body mass index ,rash ,necrosis ,030207 dermatology & venereal diseases ,0302 clinical medicine ,Blister ,Interquartile range ,adults ,Vasoconstrictor Agents ,Hospital Mortality ,Prospective Studies ,Prospective cohort study ,Skin ,SarsCoV-2 ,Acute Kidney Injury ,Middle Aged ,Morbilliform ,Rash ,Chilblains ,Hospitalization ,eruption ,030220 oncology & carcinogenesis ,Female ,Original Article ,morbilliform ,medicine.symptom ,hospitalized ,medicine.medical_specialty ,mucocutaneous ,Mucocutaneous zone ,Dermatology ,AKI, acute kidney injury ,Skin Diseases ,03 medical and health sciences ,Northwell ,Renal Dialysis ,Internal medicine ,Skin Ulcer ,medicine ,Humans ,Dialysis ,Purpura ,IQR, interquartile range ,Aged ,Mechanical ventilation ,ulcer ,Mucous Membrane ,business.industry ,SARS-CoV-2 ,COVID-19 ,Thrombosis ,Exanthema ,Respiration, Artificial ,CI, confidence interval ,business - Abstract
Background Limited information exists on mucocutaneous disease and its relation to course of COVID-19. Objective To estimate prevalence of mucocutaneous findings, characterize morphologic patterns, and describe relationship to course in hospitalized adults with COVID-19. Methods Prospective cohort study at 2 tertiary hospitals (Northwell Health) between May 11, 2020 and June 15, 2020. Results Among 296 hospitalized adults with COVID-19, 35 (11.8%) had at least 1 disease-related eruption. Patterns included ulcer (13/35, 37.1%), purpura (9/35, 25.7%), necrosis (5/35, 14.3%), nonspecific erythema (4/35, 11.4%), morbilliform eruption (4/35, 11.4%), pernio-like lesions (4/35, 11.4%), and vesicles (1/35, 2.9%). Patterns also showed anatomic site specificity. A greater proportion of patients with mucocutaneous findings used mechanical ventilation (61% vs 30%), used vasopressors (77% vs 33%), initiated dialysis (31% vs 9%), had thrombosis (17% vs 11%), and had in-hospital mortality (34% vs 12%) compared with those without mucocutaneous findings. Patients with mucocutaneous disease were more likely to use mechanical ventilation (adjusted prevalence ratio, 1.98; 95% confidence interval, 1.37-2.86); P
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- 2020
4. KIR3DS1-Specific D0 Domain Polymorphisms Disrupt KIR3DL1 Surface Expression and HLA Binding
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Tiernan J. Mulrooney, Katharine C. Hsu, Aaron C. Zhang, Jeanette E. Boudreau, and Yehuda Goldgur
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Immunology ,HEK 293 cells ,HLA-B Antigens ,Immunology and Allergy ,Plasma protein binding ,Human leukocyte antigen ,Biology ,KIR3DL1 ,Ligand (biochemistry) ,Receptor ,Molecular biology ,Epitope - Abstract
KIR3DL1 is a polymorphic inhibitory receptor that modulates NK cell activity through interacting with HLA-A and HLA-B alleles that carry the Bw4 epitope. Amino acid polymorphisms throughout KIR3DL1 impact receptor surface expression and affinity for HLA. KIR3DL1/S1 encodes inhibitory and activating alleles, but despite high homology with KIR3DL1, the activating receptor KIR3DS1 does not bind the same ligand. Allele KIR3DL1*009 resulted from a gene recombination event between the inhibitory receptor allele KIR3DL1*001 and the activating receptor allele KIR3DS1*013. This study analyzed the functional impact of KIR3DS1-specific polymorphisms on KIR3DL1*009 surface expression, binding to HLA, and functional capacity. Flow-cytometric analysis of primary human NK cells as well as transfected HEK293T cells shows that KIR3DL1*009 is expressed at a significantly lower surface density compared with KIR3DL1*001. Using recombinant proteins of KIR3DL1*001, KIR3DL1*009, and KIR3DS1*013 to analyze binding to HLA, we found that although KIR3DL1*009 displayed some evidence of binding to HLA compared with KIR3DS1*013, the binding was minimal compared with KIR3DL1*001 and KIR3DL1*005. Mutagenesis of polymorphic sites revealed that the surface phenotype and reduced binding of KIR3DL1*009 are caused by the combined amino acid polymorphisms at positions 58 and 92 within the D0 extracellular domain. Resulting from these effects, KIR3DL1*009+ NK cells exhibited significantly less inhibition by HLA-Bw4+ target cells compared with KIR3DL1*001+ NK cells. The data from this study contribute novel insight into how KIR3DS1-specific polymorphisms in the extracellular region impact KIR3DL1 surface expression, ligand binding, and inhibitory function.
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- 2015
5. Cell-extrinsic MHC class I molecule engagement augments human NK cell education programmed by cell-intrinsic MHC class I
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Bo Dupont, Dale L. Greiner, Jeanette E. Boudreau, Zeguo Zhao, Katharine C. Hsu, Aaron C. Zhang, Xiao-Rong Liu, and Leonard D. Shultz
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0301 basic medicine ,Lymphokine-activated killer cell ,biology ,Janus kinase 3 ,Cellular differentiation ,Immunology ,Human leukocyte antigen ,Major histocompatibility complex ,Article ,Cell biology ,03 medical and health sciences ,Interleukin 21 ,030104 developmental biology ,0302 clinical medicine ,Infectious Diseases ,MHC class I ,Interleukin 12 ,biology.protein ,Immunology and Allergy ,030215 immunology - Abstract
Summary The effector potential of NK cells is counterbalanced by their sensitivity to inhibition by "self" MHC class I molecules in a process called "education." In humans, interactions between inhibitory killer immunoglobulin-like receptors (KIR) and human MHC (HLA) mediate NK cell education. In HLA-B ∗ 27:05 + transgenic mice and in patients undergoing HLA-mismatched hematopoietic cell transplantation (HCT), NK cells derived from human CD34 + stem cells were educated by HLA from both donor hematopoietic cells and host stromal cells. Furthermore, mature human KIR3DL1 + NK cells gained reactivity after adoptive transfer to HLA-B ∗ 27:05 + mice or bone marrow chimeric mice where HLA-B ∗ 27:05 was restricted to either the hematopoietic or stromal compartment. Silencing of HLA in primary NK cells diminished NK cell reactivity, while acquisition of HLA from neighboring cells increased NK cell reactivity. Altogether, these findings reveal roles for cell-extrinsic HLA in driving NK cell reactivity upward, and cell-intrinsic HLA in maintaining NK cell education.
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- 2016
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