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Midwest Clinical and Translational Research Meeting of CSCTR and MWAFMR

DOI: 10.1136/jim-2022-MW Published 3 October 2022
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  • Abstract 2 Figure 1
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    Abstract 2 Figure 1

    Procedural characteristics with the use of a mixed reality head mounted display

  • Abstract 5 Figure 1
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    Abstract 5 Figure 1

    Deployed PFO closure device during procedure

  • Abstract 6 Figure 1
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    Abstract 6 Figure 1

    Bacterial phylum abundance in the intestinal microbiome

  • Abstract 6 Figure 2
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    Abstract 6 Figure 2

    Intestinal barrier dysfunction in CPB versus controls

  • Abstract 6 Figure 3
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    Abstract 6 Figure 3

    Short chain fatty acid levels in CPB versus controls

  • Abstract 6 Figure 4
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    Abstract 6 Figure 4

    Intestinal eicosanoids levels in CPB versus controls

  • Abstract 6 Figure 5
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    Abstract 6 Figure 5

    Systemic cytokine levels in CPB versus controls

  • Abstract 7 Figure 1
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    Abstract 7 Figure 1

    Mechanisms of thrombosis in patients with lipoedema and lymphedema. Platelets are hyperactivated through PAR1 agonist (TRAP6) and thromboxane receptor agonist (U46619) in both lipedema and lymphedema patients. Platelets are hyperactivated with P2Y12 receptor agonist (ADP) and GPVI receptor agonist (CRP) only in lymphedema patients

  • Abstract 7 Figure 2
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    Abstract 7 Figure 2

    Mechanisms of thrombosis in patients with lipoedema and lymphedema. Fibrin generation in platelet-deplete plasma from subjects

  • Abstract 10 Figure 1
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    Abstract 10 Figure 1

    Demographic distribution of study population

  • Abstract 10 Figure 2
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    Abstract 10 Figure 2

    Forest plot demonstrating the risk of mortality for patients on various combinations of medications (Risk Ratio *p<0.05, **p<0.01)

  • Abstract 10 Figure 3
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    Abstract 10 Figure 3

    Plot showing association of increasing age with worse outcomes (p<0.01 for all outcomes)

  • Abstract 11 Figure 1
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    Abstract 11 Figure 1

    ECG’s from second (a), third (b), and fourth (c) admissions depicting the presence and resolution of diffuse ST-elevations in anterior and inferior leads, with PR depressions in leads II, III, aVF, V5, and V6

  • Abstract 11 Figure 2
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    Abstract 11 Figure 2

    Chest X-Ray showing left-sided pleural effusion (a). CT angiogram of chest with contrast depicting pericardial effusion (b, c). Cardiac MRI demonstrating a clear demarcated circumferential rim of delayed enhancement in the pericardium (d)

  • Abstract 15 Figure 1–3
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    Abstract 15 Figure 1–3
  • Abstract 16 Figure 1
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    Abstract 16 Figure 1
  • Abstract 18 Figure 1
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    Abstract 18 Figure 1

    Te preferred reporting items for systematic review and meta-analysis (PRISMA) flow chart for the included studies

  • Abstract 18 Figure 2
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    Abstract 18 Figure 2

    Forest plot of BCG and total atopic diseases. Random effects model forest plot shows ORs and 95% Cis for the association between BCG vaccination and total atopic disease

  • Abstract 18 Figure 3
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    Abstract 18 Figure 3

    Forest plot of the association between BCG vaccination and asthma. Random effects model forest plot shows ORs and 95% Cis for the association between BCG vaccination and asthma. OR = 0.73, 95% CI 0.58 to 0.92. M-H = Mantel-Haenszel; OR = odds ratio; CI = confidence interval

  • Abstract 18 Figure 4
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    Abstract 18 Figure 4

    Forest plot of the association between BCG vaccination and rhinitis. Random effects model forest plot shows ORs and 95% CIs of the association between BCG vaccination and rhinitis. OR = 0.99, 95% CI 0.81 to 1.21. M-H = Mantel-Haenszel; OR = odds ratio; CI= confidence interval

  • Abstract 18 Figure 5
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    Abstract 18 Figure 5

    Forest plot of the association between BCG vaccination and eczema. Random effects model forest plot shows ORs and 95% Cis for the association between BCG vaccination and eczema. OR = 1.09, 95% CI 0.60 to 1.96. M-H = Mantel-Haenszel; OR = odds ratio; CI = confidence interval

  • Abstract 20 Figure 1
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    Abstract 20 Figure 1

    Left upper extremity nodular skin lesion

  • Abstract 20 Figure 2
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    Abstract 20 Figure 2

    Nodular skin lesion evolving to hemorrhagic bulla

  • Abstract 20 Figure 3
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    Abstract 20 Figure 3

    Nodular hemorrhagic bulla evolving into cribriform appearing ulcer

  • Abstract 28 Figure 1
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    Abstract 28 Figure 1

    Isoleucine restriction robustly reduces body weight in both male and female geriatric mice starting at 20 months of age. Weekly body weight records of both male (left) and female (right) aged mice starting their respective dietary intervention at 20 months of age. A robust decrease followed by stabilization within a month is seem in both isoleucine restriction groups. A decrease in body weight was also observed in the protein restriction group, but the effect size is relatively less

  • Abstract 28 Figure 2
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    Abstract 28 Figure 2

    Isoleucine restriction induces leanness in aged mice of both sexes. Small animal MRI is used to determine the% body composition of mice before dietary intervention and every 3 weeks. It was observed that both male and female mice fed an isoleucine restriction diet become much leaner than their control counterparts. The effect of a protein restriction diet appears to be lessened in female mice

  • Abstract 28 Figure 3
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    Abstract 28 Figure 3

    Isoleucine restriction improves glucose tolerance in both male and female aged mice In a glucose tolerance assay, intraperitoneal injection of glucose was better tolerated in animals fed either an isoleucine restriction diet or a protein restriction diet. The benefits of a protein restriction diet was more significant in females

  • Abstract 28 Figure 4
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    Abstract 28 Figure 4

    Isoleucine restriction induces cardiac remodeling in aged female mice In females only, echocardiogram experiments revealed a decrease in cardiac stroke volume which was compensated by an increase in heart rate

  • Abstract 28 Figure 5
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    Abstract 28 Figure 5

    Isoleucine and protein restriction exhibited distinct modulation of enzymatic phosphorylation pathways. A brief evaluation of whole heart protein phosphorylation downstream of mTORC1 found differences between male mice fed an isoleucine restriction diet and a protein restriction diet

  • Abstract 30 Figure 1
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    Abstract 30 Figure 1

    AFMR graph

  • Abstract 31 Figure 1
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    Abstract 31 Figure 1
  • Abstract 31 Figure 2
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    Abstract 31 Figure 2

    Survival kaplan-meyer curve

  • Abstract 32 Figure 1
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    Abstract 32 Figure 1

    Multiplex immunofluorescence showing significant difference in intra-tumoral versus adjacent thyroid tissue expression of PD-1, PD-L1 (p<0.05) amongst 17 patients with differentiated thyroid cancer

  • Abstract 32 Figure 2
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    Abstract 32 Figure 2

    Multiplex immunofluorescence showing more FOXP3+ T regulatory cells, CD68+ macrophages, PD-L1 expression in patient with distant metastases amongst 17 patients with differentiated thyroid cancer

  • Abstract 32 Figure 3
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    Abstract 32 Figure 3

    Multiplex immunofluorescence of a differentiated thyroid cancer tissue specimen demonstrating PD-1 staining along the leading edge of the tumor

  • Abstract 36 Figure 1
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    Abstract 36 Figure 1
  • Abstract 36 Figure 2
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    Abstract 36 Figure 2

    ‘A guide to managing your high blood pressure’ brochure

  • Abstract 36 Figure 3
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    Abstract 36 Figure 3

    ‘Signs and symptoms’ tearsheet

  • Abstract 38 Figure 1
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    Abstract 38 Figure 1

    Infectious disease specialists’ peer- review daptomycin stewardship recommendation acceptance rates. Of 183 interventions, 93 (51%) were accepted over the 5 year program implementation

  • Abstract 42 Figure 1
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    Abstract 42 Figure 1

    IHC findings in intestinal tissue of CITRO miceA) Immunohistochemistry staining for MAA antigen in the intestinal tissue of mice in the CITRO model showed significant increase compared to controls p<0.03. Represented image of 6 replicatesB) Immunohistochemistry staining for cit antigen in the intestinal tissue of mice in the CITRO model showed significant increase compared to controls p<0.001. Represented image of 6 replicatesC) Immunohistochemistry staining for Calprotectin antigen in the intestinal tissue of mice in the CITRO model showed significant increase compared to controls ***p<0.0001. Represented image of 6 replicatesD) Immunohistochemistry staining for Claudin-2 antigen in the intestinal tissue of mice in the CITRO model showed significant increase compared to controls ***p<0.001. Represented image of 6 replicatesE) Immunohistochemistry staining for CD19 antigen in the intestinal tissue of mice in the CITRO model showed significant increase compared to controls ***p<0.001. Represented image of 6 replicatesF) Immunohistochemistry co-localization between MAA, citrulline and IBD proteins in the intestinal tissue from mice in the CITRO model. R-squared value showing the amount of overlap between MAA, citrulline and IBD proteins. A significant increase in colocalization is seen between MAA and Calprotectin compared to Cit and Calprotectin ***p=0.0001. Co-localization between cit and claudin-2 was also increased compared to MAA and claudin-2 ***p<0.0001

  • Abstract 42 Figure 2
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    Abstract 42 Figure 2

    Serum Anti-MAA IgG antibodies are increased in the CITRO model compared to control mice. Anti-MAA IgG against MAA-CIT is significantly increased in the CITRO model compared to controls and to MAA and CIT alone

  • Abstract 45 Figure 1
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    Abstract 45 Figure 1

    TEER varies by GUT segment. Purple represents patients with cirrhosis and yellow represents non-cirrhotic control

  • Abstract 47 Figure 1
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    Abstract 47 Figure 1

    Mortality

  • Abstract 47 Figure 2
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    Abstract 47 Figure 2

    Mortality with subgrouping according to ACS patients’ exclusion. ACS: abdominal compartment syndrome

  • Abstract 47 Figure 3
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    Abstract 47 Figure 3

    Mortality with subgrouping according to IAH pressure cut off. IAH: intra-abdominal hypertension

  • Abstract 47 Figure 4
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    Abstract 47 Figure 4

    Multiorgan organ dysfunction syndrome

  • Abstract 47 Figure 5
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    Abstract 47 Figure 5

    Respiratory, renal and cardiovascular failure

  • Abstract 51 Figure 1
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    Abstract 51 Figure 1

    PLD2 intracellular pathway. Graphical representation of the established role PLD2 has intracellularly

  • Abstract 51 Figure 2
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    Abstract 51 Figure 2

    PEL model results

  • Abstract 51 Figure 3
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    Abstract 51 Figure 3

    MSC model results

  • Abstract 57 Figure 1
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    Abstract 57 Figure 1

    Enrollment scheme hamidi

  • Abstract 57 Figure 2
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    Abstract 57 Figure 2

    Increase in LCS participation after intervention

  • Abstract 57 Figure 3
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    Abstract 57 Figure 3

    Referral to LCS program and outcome

  • Abstract 58 Figure 1
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    Abstract 58 Figure 1

    UChicago-Moffitt adult acute lymphoblastic leukemia (ALL) cohort. (A) Demographic characteristics of 353 adult ALL patients. (B) Variant allelic fractions of mutations detected in this cohort. (C) The associations between clinical variables and pathogenic mutations are colored by odds ratio. (D) Kaplan-Meier relapse-free and overall survival curves of ALL patients stratified based on the presence of clonal hematopoiesis (CH) mutations stem cells (HSCs). If ARCH is a precursor lesion to ALL, HSCs harboring these mutations are expected to maintain hematopoiesis and give rise to mature non-malignant cells harboring similar mutations. To gain insights into the clonal architecture of hematopoiesis in ARCH-associated ALL, we performed single-cell DNA and protein sequencing using the Mission Bio, lnc. amplicon-based sequencing platform. The data from 4,258 cells of an ARCH-associated T-ALL patient are shown in Figure 2. Cells were clustered by immunophenotype, and five pathogenic mutations involving TP53, PHF6, EZH2, ETV6 and ASXL1 genes were overlayed into individual cells of 11 clusters. Most of the mature lymphoid cells residing in T-, B-, and NK-cell clusters were wild-type, whereas T-ALL blasts and myeloid cells of monocytic, megakaryocytic and granulocytic origins shared these mutations in homozygous and heterozygous states. Histopathologic examination of myeloid compartment did not reveal any signs of myeloid malignancy such as dysplasia

  • Abstract 58 Figure 2
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    Abstract 58 Figure 2

    Single-cell DNA+protein sequencing of pre-treatment bone marrow sample from an ARCH-associated T-ALL patient. (A) Uniform manifold approximation and projection (UMAP) plot of 4,258 cells clustered by immunophenotype. Key markers used to distinguish clusters are highlighted on the right. (B) Genotype for five pathogenic mutations overlayed into each cell. HOM, homozygous; HET, heterozygous; WT, wild type

  • Abstract 62 Figure 1
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    Abstract 62 Figure 1

    Chest X-ray

  • Abstract 62 Figure 2
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    Abstract 62 Figure 2

    CT chest

  • Abstract 63 Figure 1
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    Abstract 63 Figure 1
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    Abstract 63 Figure 2
  • Abstract 64 Figure 1
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    Abstract 64 Figure 1

    Peripheral blood smear on the initial presentation showing atypical monocytic cells consistent with acute monocytic leukemia

  • Abstract 65 Figure 1
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    Abstract 65 Figure 1

    Warfarin-induced calciphylaxis

  • Abstract 67 Figure 1
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    Abstract 67 Figure 1
  • Abstract 67 Figure 2
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    Abstract 67 Figure 2
  • Abstract 71 Figure 1
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    Abstract 71 Figure 1

    Left ankle magnetic resonance imaging

  • Abstract 71 Figure 2
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    Abstract 71 Figure 2

    Methenamine silver stain of ankle tissue

  • Abstract 74 Figure 1
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    Abstract 74 Figure 1

    CODEX image of glomerulitis. CD8 T cells and CD11c mononuclear phagocytes in glomerulitis in a kidney transplant biopsy

  • Abstract 75 Figure 1
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    Abstract 75 Figure 1

    Timeline of inotropic support with intervention

  • Abstract 77 Figure 1
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    Abstract 77 Figure 1
  • Abstract 80 Figure 1
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    Abstract 80 Figure 1

    A/B pre-operative X-ray of historical C3-C6 posterior spinal fusion

  • Abstract 80 Figure 2
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    Abstract 80 Figure 2

    Post-operative CT scan of CAPDF consisting of posterior spinal fusion revision (A) and C3-C6 ACDF (B)

  • Abstract 82 Figure 1
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    Abstract 82 Figure 1

    Pulse sequence diagram

  • Abstract 82 Figure 2
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    Abstract 82 Figure 2

    Timing diagram

  • Abstract 82 Figure 3
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    Abstract 82 Figure 3

    Cine and tagging pre-scan calibration sensitivity

  • Abstract 82 Figure 4
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    Abstract 82 Figure 4

    Control vs. validation

  • Abstract 82 Figure 5
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    Abstract 82 Figure 5

    Cine-tag overlay

  • Abstract 83 Figure 1
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    Abstract 83 Figure 1

    * Inpatient Day 5 – First administration of doxycycline therapy • ** Inpatient Day 9 – Final administration of doxycycline therapy • Outpatient Day 4- First follow up after hospital discharge • Marked increase in serum creatinine 24 hours after first dose of doxycycline. Serum creatinine begins to downtrend 48 hours after final dose of doxycycline

  • Abstract 83 Figure 2
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    Abstract 83 Figure 2

    Marked decrease in GFR 24 hours after doxycycline administration with near threefold increase in BUN. GFR begins to recover 48 hours after final dose of doxycycline. BUN levels begin to decline after GFR exceeds 20 mL/min

  • Abstract 83 Figure 3
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    Abstract 83 Figure 3

    Diffuse lymphocytes, monocytes and eosinophils infiltrate between the tubules and are associated with lymphocytic tubulitis. (H&E stain, 20x magnification)

  • Abstract 83 Figure 4
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    Abstract 83 Figure 4

    Tamm-Horsfall protein casts are found within tubules and show extravasation into the interstitium associated with an inflammatory infiltrate. (PAS stain, 20x magnification) contributor (figures 3 & 4)- Amy Lynn, MD vice chair of anatomic pathology consultants in laboratory medicine/promedica laboratories

  • Abstract 93 Figure 1
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    Abstract 93 Figure 1

    Multivariable model of predictors of 28 day mortality. Ordered forest plot of the predictors, including H2RA group, of mortality in our cohort of sepsis-3 patients

  • Abstract 98 Figure 1
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    Abstract 98 Figure 1

    Differential gene expression in human airway epithelial cells

  • Abstract 104 Figure 1
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    Abstract 104 Figure 1

    PCR for mRNA levels of calcium binding proteins from stimulated U-937 cells

  • Abstract 104 Figure 2
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    Abstract 104 Figure 2

    Western blot from stimulated U-937 cells

  • Abstract 105 Figures 1–6
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    Abstract 105 Figures 1–6
  • Abstract 106 Figure 1
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    Abstract 106 Figure 1

    PCR for mRNA-fold increase from stimulated U-937 macrophages

  • Abstract 106 Figure 2
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    Abstract 106 Figure 2

    ELISA for M1- associated cytokines from stimulated U-937 macrophages

  • Abstract 106 Figure 3
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    Abstract 106 Figure 3

    ELISA for M2- associated cytokines from stimulated U-937 macrophages

  • Abstract 109 Figure 1
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    Abstract 109 Figure 1
  • Abstract 110 Figure 1
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    Abstract 110 Figure 1

    Ultrasound images of bilateral pre-patellar bursitis

  • Abstract 110 Figure 2
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    Abstract 110 Figure 2

    Ultrasound-guided aspiration of bilateral pre-patellar bursaeTransverse view, anterior right knee; needle entry of pre-patellar bursa from 3 o’clock position, prior to aspiration (A) and status post aspiration (B). Hyperechoic margin along synovial lining representing calcium crystal deposition. Transverse view, anterior left knee; needle entry of pre-patellar bursa from 2–3 o’clock position, prior to aspiration (C) and status post aspiration (D)

  • Abstract 111 Figure 1
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    Abstract 111 Figure 1

    Right forearm swelling, erythema and skin tightening. Stitch marks are noted after obtaining a biopsy t months after initial encounter with the Rheumatology clinic

  • Abstract 111 Figure 2
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    Abstract 111 Figure 2

    Deep section showing the lower portion of the biopsy including the fascia. The section shows inflammation and diffuse thickening of the fascia H&E: 2x

  • Abstract 111 Figure 3
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    Abstract 111 Figure 3

    Mixed inflammation, including multiple eosinophils (arrows) in the dermis adjacent to the epidermis H&E: 20x

  • Abstract 111 Figure 4
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    Abstract 111 Figure 4

    Deep image depicting lymphocytes, histiocytes, plasma cells, and several eosinophils (encircled) in a focus of inflammation within the thickened fascial tissue. H&E: 40x

  • Abstract 112 Figure 1
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    Abstract 112 Figure 1

    CT scans showing the sagittal sections of the SMA artery before (A) and after (B) two months of treatment with steroids

Tables

  • Figures
  • Abstract 5 Table 1
  • Abstract 36 Table 1
  • Abstract 36 Table 2
  • Abstract 36 Table 3
  • Abstract 39 Table 1
  • Abstract 43 Table 1
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    Abstract 43 Table 1
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  • Abstract 43 Table 2
  • Abstract 43 Table 3
  • Abstract 44 Table 1
  • Abstract 46 Table 1
  • Abstract 46 Table 2
  • Abstract 48 Table 1
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    Abstract 48 Table 1
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  • Abstract 48 Table 2
  • Abstract 48 Table 3
  • Abstract 49 Table 1
  • Abstract 49 Table 2
  • Abstract 54 Table 1

    Antibody response rate in CLL, WM and other NHL after SARS-CoV-2 vaccination

    MalignancyAll PatientsModernaPfizerp-value*
    CLL (n = 181) 50% (91/181) 61% (44/72) 44% (47/106) 0.028
    • No Treatment (n = 79) 68% (54/79) 71% (25/35) 66% (29/44) 0.60
    • Any Treatment (n = 102) 36% (37/102)** 51% (19/37) 29% (18/62) 0.026
    • BTK Inhibitor (n = 76) 33% (25/76)** 54% (14/26) 23% (11/48) 0.0072
    † {• Anti-CD20 Ab (n = 66) 32% (21/66)** 42% (10/24) 26% (11/42) 0.19
    • BCL-2 Inhibitor (n = 30) 37% (11/30) 46% (6/13) 29% (5/17) 0.35
    WM (n = 21) 67% (14/21) 88% (7/8) 54% (7/13) 0.11
    Other NHLs (n = 38) 71% (27/38) 80% (8/10) 70% (19/27) 0.56
    • *Comparing antibody positivity in respective subgroups among patient who received either the Moderna or Pfizer vaccination. P-value calculated using chi-square testing and a value of < 0.05 is considered statistically significant. ** Some patients excluded from subsequent p-value calculation due to receiving doses from different vaccine brands. †Denotes current or prior therapy with specified CLL therapy and antibody response to vaccination. Some patients are included in multiple rows due to receiving multiple classes of treatment.

    • Ab = antibody, BCL-2 = B-cell lymphoma 2, BTK = Bruton tyrosine kinase, CLL = chronic lymphocytic leukemia, NHLs = non-Hodgkin’s lymphomas, WM = Waldenstrom macroglobulinemia

  • Abstract 70 Table 1
  • Abstract 97 Table 1
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Vol 70 Issue 7 Table of Contents
Journal of Investigative Medicine: 70 (7)
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Midwest Clinical and Translational Research Meeting of CSCTR and MWAFMR
Journal of Investigative Medicine Oct 2022, 70 (7) 1557-1657; DOI: 10.1136/jim-2022-MW

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Midwest Clinical and Translational Research Meeting of CSCTR and MWAFMR
Journal of Investigative Medicine Oct 2022, 70 (7) 1557-1657; DOI: 10.1136/jim-2022-MW
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Midwest Clinical and Translational Research Meeting of CSCTR and MWAFMR
Journal of Investigative Medicine Oct 2022, 70 (7) 1557-1657; DOI: 10.1136/jim-2022-MW
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