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Correction| Volume 179, ISSUE 1, P537-538, July 2011

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        In the article entitled “The Early Growth Response Gene Egr2 (Alias Krox20) Is a Novel Transcriptional Target of Transforming Growth Factor-β that Is Up-Regulated in Systemic Sclerosis and Mediates Profibrotic Responses” (Volume 178, pages 2077–2090 of the May 2011 issue of The American Journal of Pathology), the third author's name was listed incorrectly. The correct name is Swati Bhattacharyya.
        In the article entitled “AP-1–Mediated M2 Macrophage Infiltration Underlies IL-1β–but Not VEGF-A–Induced Lymph- and Angiogenesis” (Volume 178, pages 1913–1921 of the April 2011 issue), HLECs were defined incorrectly. The correct expansion for HLECs is human lymphatic endothelial cells. This error occurred in the print article only; the online (HTML and PDF) versions of this article appear correctly.
        In the article entitled “NF-κB Inhibition Protects against Tumor-Induced Cardiac Atrophy in Vivo” (Volume 178, pages 1059–1068 of the March 2011 issue), the fourth author's name was listed incorrectly. The correct name is Luge Li.
        In the article entitled “Bone Marrow-Derived Progenitor Cells Do Not Contribute to Podocyte Turnover in the Puromycin Aminoglycoside and Renal Ablation Models in Rats” (Volume 178, pages 494–499 of the February 2011 issue), the fourth author's surname was listed incorrectly. The correct surname name is Agustian. In addition, the author affiliation for Jan U. Becker contained errors. The correct author affiliation is Institute of Pathology, Hannover Medical School, Hannover, Germany.
        In the article entitled “CD4+ T Cells Sensitized by Vascular Smooth Muscle Induce Vasculitis, and Interferon Gamma Is Critical for the Initiation of Vascular Pathology” (Volume 177, pages 3215–3223 of the December 2010 issue), panel B was inadvertently duplicated as panel C in Figure 1.
        Figure thumbnail gr1
        Figure 1Vasculitis incidence after transfer of SMC-sensitized lymphocytes is similar in wt and in B cell-deficient (JhD) mice. AC. Vasculitis incidence scored on H&E sections of lung (each diamond depicts a mouse; horizontal bar is average). Control indicates noninjected mice. A: Adoptive transfer of wt BALB/c lymphocytes previously sensitized by co-culture (wt mL) with syngeneic SMC to wt BALB/c recipient mice; n = 11, P = 0.003 (four experiments). SM are mice injected with primary smooth muscle cultures (106 cells/mouse). Ly are mice injected with isolated naïve spleen lymphocytes (5 × 106 cells/mouse). B: Transfer of sensitized wt BALB/c lymphocytes to RAG-2-deficient mice; n = 7, P = 0.006 (three experiments). C: Transfer of sensitized JhD lymphocytes to JhD mice; n = 12 mice, P = 0.00002 (seven experiments). D: H&E staining of 4-μm paraffin section of lung 7 days after vasculitis induction in JhD mouse, showing blood vessels with granulomatous- like inflammation and infiltration of leukocytes with destruction of vessel wall. L indicates vessel lumen. Scale bar = 20 μm. Original magnification, ×400.
        In the article entitled “β-Cell Loss and β-Cell Apoptosis in Human Type 2 Diabetes Are Related to Islet Amyloid Deposition” (Volume 178, pages 2632–2640 of the June 2011 issue), Table 2 contained errors in the definition of NA. The corrected Table 2, which correctly distinguishes between parameters with no data (ND) and those with data not applicable (NA), is shown below.
        Table 2Clinicodemographic Characteristics of Individual Subjects
        Age (years)/SexBMI (kg/m2)Blood glucose (mmol/L)Diabetes duration (years)Diabetes medicationCause of death
        Diabetes group
         62/F30.98.53NDglyburide, insulinpulmonary embolism
         78/F28.37.672dietGI hemorrhage
         59/M32.67.908insulincardiac arrest
         59/M38.47.39NDinsulinleukemia
         69/F21.29.50NDmetforminmalignancy
         81/M31.45.63NDglyburide, metforminaortic dissection
         68/M27.211.42NDmetforminGI hemorrhage
         52/M26.39.07NDnonecardiopulmonary failure
         61/M29.76.8514insulinrespiratory failure
         71/F21.39.3910glyburidecoronary artery disease
         51/F41.211.11NDglyburide, insulinmalignancy
         62/M35.97.46NDinsulin in TPNabdominal hemorrhage
         80/F29.18.8920acetohexamide,insulincoronary artery disease
         61/M36.38.9212diet, glipizidesepsis
         58/M34.48.29NDinsulincoronary artery disease
         71/M37.56.5027insulinpostoperative complications
         74/F36.013.17NDunknownaspiration pneumonia
         37/M39.77.693unknowncardiomyopathy
         71/F21.6ND12glyburidecoronary artery disease
         70/F32.810.33NDoral hypoglycemic, unspecifiedabdominal hemorrhage
         69/M21.37.0610glyburidecoronary artery disease
         64/M22.56.47NDinsulinsepsis
         40/M41.210.17NDdiet, metforminpostoperative complications
         28/M35.87.671metforminmyelodysplastic syndrome
         82/M25.617.06NDglipizidesepsis
         63/F38.810.5012insulinmalignancy
         63/M26.57.11NDdietmalignancy
         68/M25.0NANDdietcardiac arrest
         82/M19.07.502dietsepsis
        Control group
         87/F33.05.14NANAvalvular heart disease
         62/M23.45.58NANAmalignancy
         34/M17.55.14NANAmalignancy
         63/F18.75.23NANAmalignancy
         54/F49.35.94NANApostoperative complications
         82/F40.94.72NANAperforated duodenal ulcer
         61/F24.35.58NANAabdominal hemorrhage
         65/M20.56.31NANAstroke
         21/F32.24.63NANApulmonary embolism
         64/M18.76.47NANAmalignancy
         65/F40.14.79NANApulmonary veno-occlusive disease
         67/M24.15.12NANAmalignancy
         52/M24.15.26NANAmalignancy
         77/F26.36.08NANAsepsis
         34/M28.85.44NANAmalignancy
         68/F18.64.86NANAmalignancy
         89/M17.86.07NANAmalignancy
         57/F19.25.87NANAmalignancy
         75/M22.64.94NANApneumonia
         66/F25.75.43NANArespiratory failure
         50/M28.05.50NANAcardiac failure
         45/M29.84.53NANAcardiac arrest
         83/F19.85.15NANAcardiac arrest
         44/F18.05.18NANAmeningitis
         20/F22.84.60NANApulmonary hypertension
         42/F34.05.39NANAsepsis
         88/F29.26.16NANArespiratory failure
         81/M27.15.56NANArespiratory failure
         58/M24.95.44NANAstroke
         19/M32.76.22NANAmalignancy
         46/F28.16.47NANAsepsis
         78/F42.43.78NANAabdominal hemorrhage
         75/M20.95.83NANAmalignancy
         72/M34.95.56NANAmultiple myeloma
         82/M32.56.06NANAsepsis
         94/M21.95.22NANAsepsis
         68/M24.05.17NANArespiratory failure
         60/M15.96.94NANArespiratory failure
         57/M22.85.56NANAcardiac arrest
        F, female; GI, gastrointestinal; M, male; ND, no data; NA, not applicable; TPN, total parenteral nutrition.

        Linked Article

        • Bone Marrow–Derived Progenitor Cells Do Not Contribute to Podocyte Turnover in the Puromycin Aminoglycoside and Renal Ablation Models in Rats
          The American Journal of PathologyVol. 178Issue 2
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            A key event in the progression of glomerular disease is podocyte loss that leads to focal and segmental glomerulosclerosis (FSGS). Because adult podocytes are postmitotic cells, podocyte replacement by bone marrow–derived progenitors could prevent podocytopenia and FSGS. This study uses double immunofluorescence for Wilms' tumor-1 and enhanced green fluorescent protein (eGFP) to examine whether an eGFP-positive bone marrow transplant can replace podocytes under normal circumstances and in 3 different rat models of FSGS: puromycin aminoglycoside nephropathy, subtotal nephrectomy, and uninephrectomy.
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        • NF-κB Inhibition Protects against Tumor-Induced Cardiac Atrophy in Vivo
          The American Journal of PathologyVol. 178Issue 3
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            Cancer cachexia is a severe wasting syndrome characterized by the progressive loss of lean body mass and systemic inflammation. It occurs in approximately 80% of patients with advanced malignancy and is the cause of 20% to 30% of all cancer-related deaths. The mechanism by which striated muscle loss occurs is the tumor release of pro-inflammatory cytokines, such as IL-1, IL-6, and TNF-α. These cytokines interact with their cognate receptors on muscle cells to enhance NF-κB signaling, which then mediates muscle loss and significant cardiac dysfunction.
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        • The Early Growth Response Gene Egr2 (Alias Krox20) Is a Novel Transcriptional Target of Transforming Growth Factor-β that Is Up-Regulated in Systemic Sclerosis and Mediates Profibrotic Responses
          The American Journal of PathologyVol. 178Issue 5
          • Preview
            Although the early growth response-2 (Egr-2, alias Krox20) protein shows structural and functional similarities to Egr-1, these two related early-immediate transcription factors are nonredundant. Egr-2 plays essential roles in peripheral nerve myelination, adipogenesis, and immune tolerance; however, its regulation and role in tissue repair and fibrosis remain poorly understood. We show herein that transforming growth factor (TGF)-β induced a Smad3-dependent sustained stimulation of Egr2 gene expression in normal fibroblasts.
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        • VAP-1–Mediated M2 Macrophage Infiltration Underlies IL-1β– but Not VEGF-A–Induced Lymph- and Angiogenesis
          The American Journal of PathologyVol. 178Issue 4
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            Vascular adhesion protein-1 (VAP-1) contributes to inflammatory and angiogenic diseases, including cancer and age-related macular degeneration. It is expressed in blood vessels and contributes to inflammatory leukocyte recruitment. The cytokines IL-1β and vascular endothelial growth factor A (VEGF-A) modulate angiogenesis, lymphangiogenesis, and leukocyte infiltration. The lymphatic endothelium expresses intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, which facilitate leukocyte transmigration into the lymphatic vessels.
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