tbuckley/cabot-search huggingface dataset:
Phase and Size Controllable Synthesis of NaYbF<sub>4</sub> Nanocrystals in Oleic Acid/ Ionic Liquid Two-Phase System for Targeted Fluorescent Imaging of Gastric Cancer
Authors: Liyuan Pan, Meng He, Jiebing Ma, Wei Tang, Guo Gao, Rong He, Haichuan Su, Daxiang Cui
Journal: Theranostics (2013)

Upconversion nanocrystals with small size and strong fluorescent signals own great potential in applications such as biomolecule-labeling, in vivo tracking and molecular imaging.Herein we reported that NaYbF 4 : 25%Gd, 2%Tm upconversion nanocrystals with small size and strong fluorescent signals were controllably synthesized by oleic acid (OA)/ ionic liquid (IL) two-phase system for targeted fluorescent imaging of gastric cancer in vivo.The optimal synthesis condition of NaYbF 4 : 25%Gd, 2%Tm upconversion nanocrystals by OA/IL two-phase system was established, adding more metal ion such as Na + ion could facilitate the size control and crystal-phase transition, more importantly, markedly enhancing fluorescent intensity of beta-phase nanocrystals compared with traditional methods.Alpha-phase NaYbF 4 , 2%Tm upconversion nanocrystals with less than 10nm in diameter and beta-phase NaYbF 4 : 25%Gd, 2%Tm upconversion nanocrystals with 30 nm or so in diameter and strong fluorescent signals were obtained, these synthesized nanocrystals exhibited very low cytotoxicity.Folic acid-conjugated silica-modified beta-phase NaYbF 4 : 25%Gd, 2%Tm upconversion nanocrystals were prepared, could actively target gastric cancer tissues implanted into nude mice in vivo, and realized targeted fluorescent imaging.Folic acid-conjugated silica-modified NaYbF 4 : 25%Gd, 2%Tm upconversion nanocrystals show great potential in applications such as targeted near infared radiation fluorescent imaging, magnetic resonance imaging and targeted therapy of gastric cancer in the near future.
Transgenic α1A-adrenergic activation limits post-infarct ventricular remodeling and dysfunction and improves survival
Authors: X DU, X GAO, H KIRIAZIS, X MOORE, Z MING, Y SU, A FINCH, R HANNAN, A DART, R GRAHAM
Journal: Cardiovascular Research (2006)

Objective: Myocardial contractility is enhanced in transgenic (TG) mice with cardiac-restricted overexpression of the α1A-adrenergic receptors (α1A-AR). We tested the hypothesis that this enhanced inotropy protects against dysfunction and remodeling after myocardial infarction (MI).
Detection of Wilms' Tumor Antigen–Specific CTL in Tumor-Draining Lymph Nodes of Patients with Early Breast Cancer
Authors: Roopinder Gillmore, Shao-An Xue, Angelika Holler, Jaspal Kaeda, Dimitri Hadjiminas, Vourneen Healy, Roberto Dina, Suzanne C. Parry, Ilaria Bellantuono, Yasmeen Ghani, R. Charles Coombes, Jonathan Waxman, Hans J. Stauss
Journal: Clinical Cancer Research (2006)

The Wilms' tumor antigen (WT1) is overexpressed in approximately 90% of breast tumors and, thus, is a potential target antigen for the immunotherapy of breast cancer. We have tested the working hypotheses that WT1 can be immunogenic in patients with breast cancer and can stimulate CTL of sufficient avidity to kill tumor cells.
A Phase II Trial of Neoadjuvant Docetaxel and Capecitabine for Locally Advanced Breast Cancer
Authors: Peter F. Lebowitz, Jennifer Eng-Wong, Sandra M. Swain, Arlene Berman, Maria J. Merino, Catherine K. Chow, David Venzon, Farah Zia, David Danforth, Edison Liu, JoAnne Zujewski
Journal: Clinical Cancer Research (2004)

Abstract Purpose: This study evaluated the toxicity and efficacy of docetaxel/capecitabine as neoadjuvant treatment for stage 2/3 breast cancer. Experimental Design: Subjects with newly diagnosed invasive stage 2 and 3 breast cancer were eligible. The first cohort of patients was treated at dose A with neoadjuvant docetaxel (75 mg/m2 i.v. day 1) and capecitabine (1000 mg/m2 orally twice daily days 2–15) for four cycles. A second cohort of subjects was treated with a reduced dose, dose B, of docetaxel (60 mg/m2 i.v. day 1) and capecitabine (937.5 mg/m2 orally twice daily days 2–15). Results: Thirty patients were enrolled. Eight of 10 patients treated at dose A required dose reductions of either docetaxel or capecitabine secondary to grade 3 or 4 toxicities: mucositis (1), hand-foot syndrome (3), diarrhea (2), perirectal abscess (1), and neutropenia (2). Because of a high rate of dose reductions, the next 20 patients were treated at dose B. The mean cumulative administered dose of docetaxel was 285 and 231 mg/m2 at dose A and dose B, respectively. For capecitabine, the mean cumulative dose at dose A and B were similar at 1585 and 1627 mg/m2/day, respectively. The overall clinical response rate was 90% with 31% of patients having a complete response and 59% having a partial response. A pathological complete response in the breast was achieved in 10% of patients after four cycles of docetaxel/capecitabine. Conclusions: Docetaxel/capecitabine is a highly active regimen in the neoadjuvant setting. Neoadjuvant therapy with 75 mg/m2 docetaxel and 1600 mg/m2/day days 2–15 is recommended.
Surgical Intervention in Terminal Illness—Doing Everything
Authors: Tyson A. Oberndorfer, Debra L. Anoff, Heidi L. Wald
Journal: JAMA Internal Medicine (2015)

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FcϵRI-mediated thymic stromal lymphopoietin production by interleukin-4-primed human mast cells
Authors: Y. Okayama, S. Okumura, H. Sagara, K. Yuki, T. Sasaki, N. Watanabe, M. Fueki, K. Sugiyama, K. Takeda, T. Fukuda, H. Saito, C. Ra
Journal: European Respiratory Journal (2009)

A significant increase of mRNA expression of thymic stromal lymphopoietin (TSLP) has been reported in the bronchial mast cells (MCs) of asthmatic subjects; however, the mechanism underlying the upregulation of TSLP mRNA and protein remains unknown. FcϵRI-mediated activation of human MCs upregulated TSLP mRNA expression by 5.2±2.9-fold, while activation of the MCs using lipopolysaccharide and polyriboinosinic:polyribocytidylic acid failed to upregulate TSLP. Stimulation of MCs with interleukin (IL)-4 alone did not affect the TSLP mRNA expression, while pre-incubation of MCs with IL-4 for 48 h significantly enhanced the FcϵRI-mediated TSLP mRNA expression (by 53.7±15.9-fold; p&lt;0.05) and the amount of TSLP in the cell pellets increased significantly from 23.4±4.3 pg·mL −1 to 121.5±3.7 pg·mL −1 (p&lt;0.0001). However, the released TSLP was rapidly degraded by proteases that were released by MCs. We identified the population of cells expressing TSLP in the lungs of 16 asthmatic and 11 control subjects by immunohistochemistry. The percentage of TSLP-positive MCs in the total population of MCs was significantly increased in asthmatic airways (p&lt;0.0001). Thus, MCs are able to store TSLP intracellularly and to produce TSLP following aggregation of FcϵRI in the presence of IL-4.
p53 protein expression in viral warts from patients with epidermodysplasia verruciformis
Authors: A. PIZARRO, C. GAMALLO, J.S. CASTRKSANA, L. GOMEZ, J. PALACIOS, N. BENITO, J. ESPADA, E. FONSECA, F. CONTRERAS
Journal: British Journal of Dermatology (2006)

The p53 protein is the product of a tumour suppressor gene, which is implicated in many human malignancies. p53 expression was investigated by immunohistochemistry in a series of viral warts (n = 12) from five patients with epidermodysplasia verruciformis (EV), using a monoclonal anti‐p53 antibody (D07). p53 expression was also investigated in a series of common warts (n = 8), flat warts (n= 8), and penile bowenoid papulosis (n = 6) from non‐EV patients. Immunostaining was positive in 11 of 12 (92%) EV warts, whereas p53 reactivity was negative in most cases of warts from non‐EV patients. Exons 5–8 of the p53 gene were screened by the polymerase chain reaction‐single strand conformation polymorphism technique in four EV warts, which were strongly stained for p53, and p53 mutations were not detected. These results suggest an association between p53 accumulation (probably of wild type) and EV warts.
Activation of p53 Promotes Renal Injury in Acute Aristolochic Acid Nephropathy
Authors: Li Zhou, Ping Fu, Xiao R. Huang, Fei Liu, Kar Neng Lai, Hui Y. Lan
Journal: Journal of the American Society of Nephrology (2009)

Ingestion of aristolochic acid (AA) can cause AA nephropathy (AAN), in which excessive death of tubular epithelial cells (TECs) characterize the acute phase. AA forms adducts with DNA, which may lead to TEC apoptosis via p53-mediated signaling. We tested this hypothesis both by studying p53-deficient mice and by blocking p53 in TECs with its inhibitor pifithrin-alpha. AA induced acute AAN in wild-type mice, resulting in massive apoptotic and necrotic TEC death and acute renal failure; p53 deficiency or pharmacologic inhibition attenuated this injury. In vitro, AA induced apoptotic and necrotic death of TEC in a time- and dosage-dependent manner, with apoptosis marked by a 10-fold increase in cleaved caspase-3 and terminal deoxynucleotidyl transferase-mediated digoxigenin-deoxyuridine nick-end labeling-positive/Annexin V-positive propidium iodide-negative TECs (all P < 0.001). AA induced dephosphorylation of STAT3 and the subsequent activation of p53 and TEC apoptosis. In contrast, overexpression of STAT3, p53 inhibition, or p53 knockdown with small interfering RNA all attenuated AA-induced TEC apoptosis. Taken together, these results suggest that AA induces TEC death via apoptosis by dephosphorylation of STAT3 and posttranslational activation of p53, supporting the hypothesis that p53 promotes renal injury in acute AAN.
Spread of extensively resistant VIM-2-positive ST235 Pseudomonas aeruginosa in Belarus, Kazakhstan, and Russia: a longitudinal epidemiological and clinical study
Authors: Mikhail V Edelstein, Elena N Skleenova, Oksana V Shevchenko, Jimson W D'souza, Dmitry V Tapalski, Ilya S Azizov, Marina V Sukhorukova, Roman A Pavlukov, Roman S Kozlov, Mark A Toleman, Timothy R Walsh
Journal: The Lancet Infectious Diseases (2013)
The validation of a novel activity monitor in the measurement of posture and motion during everyday activities
Authors: P M Grant, C G Ryan, W W Tigbe, M H Granat
Journal: British Journal of Sports Medicine (2006)

Accurate measurement of physical activity patterns can be used to identify sedentary behaviour and may facilitate interventions aimed at reducing inactivity.To evaluate the activPAL physical activity monitor as a measure of posture and motion in everyday activities using observational analysis as the criterion standard.Wearing three activPAL monitors, 10 healthy participants performed a range of randomly assigned everyday tasks incorporating walking, standing and sitting. Each trial was captured on a digital camera and the recordings were synchronised with the activPAL. The time spent in different postures was visually classified and this was compared with the activPAL output.Intraclass correlation coefficients (ICC 2,1) for interdevice reliability ranged from 0.79 to 0.99. Using the Bland and Altman method, the mean percentage difference between the activPAL monitor and observation for total time spent sitting was 0.19% (limits of agreement -0.68% to 1.06%) and for total time spent upright was -0.27% (limits of agreement -1.38% to 0.84%). The mean difference for total time spent standing was 1.4% (limits of agreement -6.2% to 9.1%) and for total time spent walking was -2.0% (limits of agreement -16.1% to 12.1%). A second-by-second analysis between observer and monitor found an overall agreement of 95.9%.The activPAL activity monitor is a valid and reliable measure of posture and motion during everyday physical activities.
Extracellular Signal–Regulated Kinase 5: A Potential Therapeutic Target for Malignant Mesotheliomas
Authors: Arti Shukla, Jill M. Miller, Christopher Cason, Mutlay Sayan, Maximilian B. MacPherson, Stacie L. Beuschel, Jedd Hillegass, Pamela M. Vacek, Harvey I. Pass, Brooke T. Mossman
Journal: Clinical Cancer Research (2013)

Abstract Purpose: Malignant mesothelioma is a devastating disease with a need for new treatment strategies. In the present study, we showed the importance of extracellular signal–regulated kinase 5 (ERK5) in malignant mesothelioma tumor growth and treatment. Experimental Design: ERK5 as a target for malignant mesothelioma therapy was verified using mesothelial and mesothelioma cell lines as well as by xenograft severe combined immunodeficient (SCID) mouse models. Results: We first showed that crocidolite asbestos activated ERK5 in LP9 cells and mesothelioma cell lines exhibit constitutive activation of ERK5. Addition of doxorubicin resulted in further activation of ERK5 in malignant mesothelioma cells. ERK5 silencing increased doxorubicin-induced cell death and doxorubicin retention in malignant mesothelioma cells. In addition, shERK5 malignant mesothelioma lines exhibited both attenuated colony formation on soft agar and invasion of malignant mesothelioma cells in vitro that could be related to modulation of gene expression linked to cell proliferation, apoptosis, migration/invasion, and drug resistance as shown by microarray analysis. Most importantly, injection of shERK5 malignant mesothelioma cell lines into SCID mice showed significant reduction in tumor growth using both subcutaneous and intraperitoneal models. Assessment of selected human cytokine profiles in peritoneal lavage fluid from intraperitoneal shERK5 and control tumor-bearing mice showed that ERK5 was critical in regulation of various proinflammatory (RANTES/CCL5, MCP-1) and angiogenesis-related (interleukin-8, VEGF) cytokines. Finally, use of doxorubicin and cisplatin in combination with ERK5 inhibition showed further reduction in tumor weight and volume in the intraperitoneal model of tumor growth. Conclusion: ERK5 inhibition in combination with chemotherapeutic drugs is a beneficial strategy for combination therapy in patients with malignant mesothelioma. Clin Cancer Res; 19(8); 2071–83. ©2013 AACR.
Genetic associations with thalidomide mediated venous thrombotic events in myeloma identified using targeted genotyping
Authors: David C. Johnson, Sophie Corthals, Christine Ramos, Antje Hoering, Kim Cocks, Nicholas J. Dickens, Jeff Haessler, Harmut Goldschmidt, J. Anthony Child, Sue E. Bell, Graham Jackson, Dalsu Baris, S. Vincent Rajkumar, Faith E. Davies, Brian G. M. Durie, John Crowley, Pieter Sonneveld, Brian Van Ness, Gareth J. Morgan
Journal: Blood (2008)
Stem Cell–Derived Nodal-Like Cardiomyocytes as a Novel Pharmacologic Tool: Insights from Sinoatrial Node Development and Function
Authors: Andrea Barbuti, Richard B. Robinson
Journal: Pharmacological Reviews (2015)

Since the first reports on the isolation and differentiation of stem cells, and in particular since the early success in driving these cells down a cardiac lineage, there has been interest in the potential of such preparations in cardiac regenerative therapy. Much of the focus of such research has been on improving mechanical function after myocardial infarction; however, electrophysiologic studies of these preparations have revealed a heterogeneous mix of action potential characteristics, including some described as "pacemaker" or "nodal-like," which in turn led to interest in the therapeutic potential of these preparations in the treatment of rhythm disorders; several proof-of-concept studies have used these cells to create a biologic alternative to electronic pacemakers. Further, there are additional potential applications of a preparation of pacemaker cells derived from stem cells, for example, in high-throughput screens of new chronotropic agents. All such applications require reasonably efficient methods for selecting or enriching the "nodal-like" cells, however, which in turn depends on first defining what constitutes a nodal-like cell since not all pacemaking cells are necessarily of nodal lineage. This review discusses the current state of the field in terms of characterizing sinoatrial-like cardiomyocytes derived from embryonic and induced pluripotent stem cells, markers that might be appropriate based on the current knowledge of the gene program leading to sinoatrial node development, what functional characteristics might be expected and desired based on studies of the sinoatrial node, and recent efforts at enrichment and selection of nodal-like cells.
Fcα Receptor (Cd89) Mediates the Development of Immunoglobulin a (Iga) Nephropathy (Berger's Disease)
Authors: Pierre Launay, Béatrice Grossetête, Michelle Arcos-Fajardo, Emmanuelle Gaudin, Sonia P. Torres, Lucie Beaudoin, Natacha Patey-Mariaud de Serre, Agnès Lehuen, Renato C. Monteiro
Journal: The Journal of Experimental Medicine (1999)

The pathogenesis of immunoglobulin A (IgA) nephropathy (IgAN), the most prevalent form of glomerulonephritis worldwide, involves circulating macromolecular IgA1 complexes. However, the molecular mechanism(s) of the disease remain poorly understood. We report here the presence of circulating soluble FcαR (CD89)-IgA complexes in patients with IgAN. Soluble CD89 was identified as a glycoprotein with a 24-kD backbone that corresponds to the expected size of CD89 extracellular domains. To demonstrate their pathogenic role, we generated transgenic (Tg) mice expressing human CD89 on macrophage/monocytes, as no CD89 homologue is found in mice. These mice spontaneously developed massive mesangial IgA deposition, glomerular and interstitial macrophage infiltration, mesangial matrix expansion, hematuria, and mild proteinuria. The molecular mechanism was shown to involve soluble CD89 released after interaction with IgA. This release was independent of CD89 association with the FcRγ chain. The disease was induced in recombination activating gene (RAG)2−/− mice by injection of serum from Tg mice, and in severe combined immunodeficiency (SCID)-Tg mice by injection of patients' IgA. Depletion of soluble CD89 from serum abolished this effect. These results reveal the key role of soluble CD89 in the pathogenesis of IgAN and provide an in vivo model that will be useful for developing new treatments.
CCR7 provides localized access to IL-2 and defines homeostatically distinct regulatory T cell subsets
Authors: Kate S. Smigiel, Elizabeth Richards, Shivani Srivastava, Kerri R. Thomas, Jan C. Dudda, Kimberly D. Klonowski, Daniel J. Campbell
Journal: The Journal of Experimental Medicine (2013)

Immune tolerance and activation depend on precise control over the number and function of immunosuppressive Foxp3+ regulatory T (T reg) cells, and the importance of IL-2 in maintaining tolerance and preventing autoimmunity is clear. However, the homeostatic requirement for IL-2 among specific populations of peripheral T reg cells remains poorly understood. We show that IL-2 selectively maintains a population of quiescent CD44loCD62Lhi T reg cells that gain access to paracrine IL-2 produced in the T cell zones of secondary lymphoid tissues due to their expression of the chemokine receptor CCR7. In contrast, CD44hiCD62LloCCR7lo T reg cells that populate nonlymphoid tissues do not access IL-2–prevalent regions in vivo and are insensitive to IL-2 blockade; instead, their maintenance depends on continued signaling through the co-stimulatory receptor ICOS (inducible co-stimulator). Thus, we define a fundamental homeostatic subdivision in T reg cell populations based on their localization and provide an integrated framework for understanding how T reg cell abundance and function are controlled by unique signals in different tissue environments.
Dietary treatment of atherosclerosis abolishes hyperresponsiveness to serotonin: implications for vasospasm.
Authors: D D Heistad, A L Mark, M L Marcus, D J Piegors, M L Armstrong
Journal: Circulation Research (1987)

Diet-induced atherosclerosis in primates impairs vasodilator responses and greatly potentiates vasoconstrictor responses to serotonin. Serotonin may play an important role in the pathogenesis of vasospasm. In diet-induced regression of atherosclerosis, intimal lesions are reduced, but maximal vasodilator responses do not improve, perhaps because of vascular fibrosis. Our goal was to determine whether dietary treatment of atherosclerosis reverses the augmented vasoconstrictor responses to serotonin and thus might reduce susceptibility to vasospasm. Normal cynomolgus monkeys, atherosclerotic monkeys, and atherosclerotic monkeys that were given a normal (regression) diet for 18 months were studied. Morphometric studies indicated that the regression diet reduced lesions in the iliac and femoral artery since intimal area was reduced by about 50%. In the hind limb perfused at constant flow, residual resistance during maximal vasodilatation produced by infusion of adenosine tended to be greater in atherosclerotic monkeys than in normals and failed to improve in regression monkeys. In contrast, vasoconstrictor responses to serotonin were greatly potentiated in atherosclerotic monkeys and were restored to normal in regression monkeys. Serotonin (20 micrograms i.a.) decreased hind limb resistance (in mm Hg/ml/min) 0.34 +/- 0.06 (mean +/- SE) in normal monkeys, increased resistance 0.58 +/- 0.17 in atherosclerotic monkeys (p less than 0.05 vs. normal), and decreased resistance 0.70 +/- 0.15 in regression monkeys (p less than 0.05 vs. atherosclerotic). Thus, dietary treatment of atherosclerosis abolishes augmented vasoconstrictor responses to serotonin. It is proposed that treatment of atherosclerosis may be beneficial, even when vasodilator responses fail to improve, by reducing susceptibility to serotonin-induced vasospasm.