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In the article entitled, “Elevated Expression of Fn14 in Non-Small Cell Lung Cancer Correlates with Activated EGFR and Promotes Tumor Cell Migration and Invasion” (Volume 181, pages 111–120 of the July 2012 issue of The American Journal of Pathology), the author footnotes contained errors. The support footnote and author contribution footnote should have read as follows:
This work was supported in part by NIH grants R01 NS055126 (J.A.W.), R01 CA130940 (N.L.T.), R01 CA103956 (J.C.L.); by the Translational Genomics Research Institute Foundation and Scottsdale Healthcare Foundation (G.J.W.), St. Joseph's Foundation (Phoenix, AZ) for the Heart and Lung Institute Research Initiative (L.J.I. and R.M.B.), and T32 HL007698 (University of Maryland School of Medicine to E.C.).
N.L.T. and J.A.W. contributed equally as senior authors on this work.
In the article entitled, “MicroRNA 15a, Inversely Correlated to PKCα, Is a Potential Marker to Differentiate between Benign and Malignant Renal Tumors in Biopsy and Urine Samples” (Volume 180, pages 1787–1797 of the May 2012 issue), the ninth author's name was listed incorrectly. The correct name is Udo Engelmann.
In the article entitled “Activated B Cells in the Granulomas of Nonhuman Primates Infected with Mycobacterium tuberculosis” (Volume 181, pages 508–514 of the August 2012 issue), the authors inadvertently omitted a funding source. J.L.F. was also supported by NIH grant R01-AI094745.
In the article entitled, “New Human Antibody Fragments Homing to Atherosclerotic Endothelial and Subendothelial Tissues: An in Vivo Phage Display Targeting Human Antibodies Homing to Atherosclerotic Tissues” (Volume 180, pages 2576–2589 of the June 2012 issue), the title was incorrect. The correct title is “In Vivo Phage Display to Identify New Human Antibody Fragments Homing to Atherosclerotic Endothelial and Subendothelial Tissues.”
In the article entitled “The Synaptic Accumulation of Hyperphosphorylated Tau Oligomers in Alzheimer Disease Is Associated With Dysfunction of the Ubiquitin-Proteasome System” (Volume 181, pages 1426-1435 of the October 2012 issue), Figure 4B, page 1430, contained an error. The authors inadvertently duplicated the bottom right images of Figure 4A, illustrating control synapses, in the right half of panel B, labeled as AD synapses. The correction of the mistake does not alter the conclusions of the article. The corrected Figure 4 (with legend) appears on page 1890.
Figure 4A: Control brain synaptoneurosomes fixed on glass slides were immunostained against presynaptic marker vGlut1, postsynaptic marker MAP2, and total tau (DA9 antibody). Magnifications of boxed areas represent tau immunoreactivity at individual synapses. Top, postsynaptic; bottom, pre- and postsynaptic. B: Tau proteins are also detected at presynaptic and postsynaptic terminals from brains affected by AD. C: Quantification of the percentage of synaptic terminals positive for tau in control (4 cases, 400 presynapses, 276 postsynapses) and AD temporal cortices (4 cases, 400 presynapses, 287 postsynapses). No significant difference was found by two-way analysis of variance. Error bars represent SEM. D: Co-localization of PSD95 and MAP2 at postsynaptic sites. Scale bars = 1 μm (A–D).
In Alzheimer disease (AD), deposition of neurofibrillary tangles and loss of synapses in the neocortex and limbic system each correlate strongly with cognitive impairment. Tangles are composed of misfolded hyperphosphorylated tau proteins; however, the link between tau abnormalities and synaptic dysfunction remains unclear. We examined the location of tau in control and AD cortices using biochemical and morphologic methods. We found that, in addition to its well-described axonal localization, normal tau is present at both presynaptic and postsynaptic terminals in control human brains.
NF-κB signal transduction is a potential therapeutic target in many malignant tumors. We have recently shown, in malignant renal proximal tumor cells, that a transcription complex, consisting of NF-κB p65 and mitogen-activated protein kinase p38α, joined by protein kinase C (PKC) α, transmigrates into the nucleus. There, PKCα suppresses the nuclear release of primary microRNA (pri-miRNA) 15a. Induced by endothelin (ET)-1, a decrease in PKCα levels leads to increased miRNA 15a (miR-15A) expression.
In vivo phage display selection is a powerful strategy for directly identifying agents that target the vasculature of normal or diseased tissues in living animals. We describe here a new in vivo biopanning strategy in which a human phage single-chain antibody (scFv) library was injected into high-fat diet-fed ApoE−/− mice. Extracellular and internalized phage scFvs were selectively recovered from atherosclerotic vascular endothelium and subjacent tissues. After three successive biopanning rounds, a panel of six clones with distinct gene sequences was isolated.
Lung cancer is the leading cause of cancer deaths worldwide; approximately 85% of these cancers are non-small cell lung cancer (NSCLC). Patients with NSCLC frequently have tumors harboring somatic mutations in the epidermal growth factor receptor (EGFR) gene that cause constitutive receptor activation. These patients have the best clinical response to EGFR tyrosine kinase inhibitors (TKIs). Herein, we show that fibroblast growth factor–inducible 14 (Fn14; TNFRSF12A) is frequently overexpressed in NSCLC tumors, and Fn14 levels correlate with p-EGFR expression.
In an attempt to contain Mycobacterium tuberculosis, host immune cells form a granuloma as a physical and immunological barrier. To date, the contribution of humoral immunity, including antibodies and specific functions of B cells, to M. tuberculosis infection in humans remains largely unknown. Recent studies in mice show that humoral immunity can alter M. tuberculosis infection outcomes. M. tuberculosis infection in cynomolgus macaques recapitulates essentially all aspects of human tuberculosis.
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