bluuebunny/crossref_metadata_2025_split huggingface dataset:
E-001 Partial central retinal artery occlusion following para-ophthalmic artery embolization: a case report
Authors: Chowdhry S , Sharma J , Blackham K 
Published: July 2011

BackgroundCoil embolization of para-ophthalmic artery aneurysms can result in acute as well as delayed visual complications. Progressive visual changes have been have been ascribed to mass effect from aneurysm thrombosis or peri-aneurysmal inflammation or edema. Abrupt, fixed visual changes are likely secondary to thromboembolic complications which result in retinal infarcts via the ophthalmic artery. Although thromboembolic complications are well described in general, clinical reports of retinal infarcts following coil embolization are rare in the literature. Thromboembolic complications resulting in central or branch retinal artery occlusion may occur in a delayed fashion following the coiling procedure.Case ReportA 43-year-old woman presented for elective coil embolization of an unruptured right para-ophthalmic artery aneurysm, measuring 7 by 7 mm with a 4 mm neck and projecting superiorly. The origin of the ophthalmic artery was located immediately inferomedial to the neck of the aneurysm. The embolization procedure was uneventful and accomplished with stent-assisted coiling utilizing predominantly Cerecyte coils. Systemic heparinization was used during the procedure, and Plavix was administered both 7 days before the procedure and continued after the procedure. About 12 h following the procedure she complained of right-sided positive visual phenomena followed by a headache. She was found to have a visual field defect OD but it was felt that the visual loss was most likely secondary to compressive optic neuropathy and she was discharged home on oral steroids. She returned to clinic 4 days later stating that her vision was not improving. Ophthalmologic exam revealed dense nasal and central defects OD, and full fields OS. Extensive areas of retinal infarction OD were seen on dilated fundus exam with the suggestion of subtle platelet-fibrin emboli. It was felt that the cause was likely artery-to-artery embolism resulting in partial central retinal artery occlusion following the coiling procedure. Vasospasm was considered but felt to be less likely. The symptoms did not resolve with oral verapamil and timolol eye drops.ConclusionOur case highlights the rare but potential complication of central or branch retinal artery occlusion from the endovascular treatment of para-ophthalmic artery aneurysms. Along with mass effect from aneurysm thrombosis or peri-aneurysmal edema, it remains an uncommon but serious cause of morbidity in these patients.
Neutrophil gelatinase-associated lipocalin in gastric carcinoma cells and its induction by TPA are controlled by C/EBPβ
Authors: Du Ze-Peng , Yuan Hua-Min , Wu Bing-Li , Chang Jing-Xia , Lv Zhuo , Shen Jian , Wu Jian-Yi , Chen Hai-Bin , Li En-Min , Xu Li-Yan 
Published: July 2011

Neutrophil gelatinase-associated lipocalin (NGAL) expression has been found to be upregulated in a variety of tumors, but the mechanism of NGAL elevation in gastric carcinoma remains unknown. Here, immunohistochemistry was applied to analyze NGAL expression in gastric carcinoma patients. Reverse transcription PCR, Western blot, and enzyme-linked immunosorbent assay (ELISA) were performed to evaluate NGAL mRNA and protein levels before and after 12-O-tetradecanoylphorbol-13-acetate (TPA) induction. Luciferase reporter assay was carried out to identify the core cis element in NGAL promoter. The binding ability and specificity of transcription factors were analyzed by electrophoretic mobility-shift assay (EMSA) and chromatin immunoprecipitation (ChIP), respectively. Results showed that NGAL was overexpressed in gastric tumor tissues. Gastric cancer cells treated with TPA resulted in the transactivation of NGAL promoter and the upregulation of its mRNA and protein levels. We identified the −110 to −79 sequence segment upstream from the transcription initiation site of NGAL as a TPA responsive element (TRE) and confirmed that C/EBPβ was able to bind to the −87 to −79 segment. Forced expression of C/EBPβ significantly increased the promoter activity of NGAL as well as its mRNA level. These results suggest that NGAL is overexpressed in gastric cancer, the binding of C/EBPβ to the TRE of its gene promoter mediates its TPA-induced overexpression in gastric carcinoma cells.
The lipopolysaccharide core ofActinobacillus suisand its relationship to those ofActinobacillus pleuropneumoniae
Authors: Ganeshapillai Jeyabarathy , Boncheff Alexander G. , Slavic Durda , MacInnes Janet , Monteiro Mario A. 
Published: July 2011

The Gram-negative bacteria Actinobacillus suis colonizes the upper respiratory and genital tracts of swine. Along with capsular polysaccharides, lipopolysaccharides (O-chain→core→lipid A~cell) are a main cell-surface component of A. suis. In this study, we determined that A. suis lipopolysaccharide incorporates a conserved core that shares some structural features with several core types of A. pleuropneumoniae . These common core structural features likely account for the observed serological cross-reactivity between A. suis and A. pleuropneumoniae, and the data suggest that the structural epitopes responsible for immunogenicity are those in the outer core domain.
Engagement of I-Branching β-1, 6-N-Acetylglucosaminyltransferase 2 in Breast Cancer Metastasis and TGF-β Signaling
Authors: Zhang Haijun , Meng Fanyan , Wu Sherwin , Kreike Bas , Sethi Seema , Chen Wei , Miller Fred R. , Wu Guojun 
Published: July 2011

Abstract
In this study, we have showed that GCNT2, a gene-encoding glucosaminyl (N-acetyl) transferase 2, I-branching enzyme, is overexpressed in highly metastatic breast cancer cell lines of human and mouse origin and basal-like breast tumor samples. GCNT2 expression is also significantly correlated to the metastatic phenotype in breast tumor samples. Functional studies showed that ectopic expression of GCNT2 enhances cell detachment, adhesion to endothelial cells, cell migration and invasion in vitro, and lung metastasis of breast cancer cells in vivo. Knockdown of GCNT2 expression decreases cell migration and invasion in vitro and lung metastasis in vivo. We have further shown the involvement of GCNT2 in the epithelial-to-mesenchymal transition (EMT). Specifically, the expression of E-cadherin is significantly changed upon GCNT2 expression at the protein level but not at the RNA level. Moreover, we have shown that GCNT2 is a direct target of the TGF-β–smad pathway and that change in GCNT2 expression modulates EMT induced by TGF-β1 treatment. Finally, we have shown that diminution of the glycosyltransferase activity of I-branching β-1, 6-N-acetylglucosaminyl transferase 2 (GCNT2) abrogates its cell migration and invasion-promoting function and synergistic effect with TGF-β to induce EMT. Our study for the first time showed that GCNT2 is a novel gene contributing to breast cancer metastasis with preferential expression in basal-like breast cancer. Moreover, we discovered that involvement of GCNT2 in EMT and TGF-β signaling, and further glycosylation modification of E-cadherin by GCNT2, are the underlying integrative mechanisms for breast cancer metastasis, implying that blocking TGF-β/GCNT2 signaling is a promising approach for targeting metastatic breast cancer. Cancer Res; 71(14); 4846–56. ©2011 AACR.
Early Tumor Progression Associated with Enhanced EGFR Signaling with Bortezomib, Cetuximab, and Radiotherapy for Head and Neck Cancer
Authors: Argiris Athanassios , Duffy Austin G. , Kummar Shivaani , Simone Nicole L. , Arai Yoshio , Kim Seungwon W. , Rudy Susan F. , Kannabiran Vishnu R. , Yang Xinping , Jang Minyoung , Chen Zhong , Suksta Nanette , Cooley-Zgela Theresa , Ramanand Susmita G. , Ahsan Aarif , Nyati Mukesh K. , Wright John J. , Van Waes Carter 
Published: July 2011

Abstract
Purpose: A phase I clinical trial and molecular correlative studies were conducted to evaluate preclinical evidence for combinatorial activity of the proteasome inhibitor bortezomib, the epidermal growth factor receptor (EGFR) inhibitor cetuximab, and radiation therapy.
Experimental Design: Patients with radiotherapy-naive stage IV or recurrent squamous cell carcinoma of the head and neck (SCCHN) were studied. Escalating doses of bortezomib (0.7, 1.0, and 1.3 mg/m2) were given intravenously twice weekly on days 1, 4, 8, and 11, every 21 days, with weekly cetuximab beginning 1 week prior and concurrently with intensity-modulated radiotherapy, delivered in 2 Gy fractions to 70 to 74 Gy. Molecular effects were examined in serial serum and SCCHN tumor specimens and the cell line UMSCC-1.
Results: Seven patients were accrued before the study was terminated when five of six previously untreated patients with favorable prognosis oropharyngeal SCCHN progressed within 1 year (progression-free survival = 4.8 months; 95% CI, 2.6–6.9). Three patients each received bortezomib 0.7 or 1.0 mg/m2, without dose-limiting toxicities; one patient treated at 1.3 mg/m2 was taken off study due to recurring cetuximab infusion reaction and progressive disease (PD). Expected grade 3 toxicities included radiation mucositis (n = 4), dermatitis (n = 4), and rash (n = 1). SCCHN-related cytokines increased in serial serum specimens of patients developing PD (P = 0.029). Bortezomib antagonized cetuximab- and radiation-induced cytotoxicity, degradation of EGFR, and enhanced prosurvival signal pathway activation in SCCHN tumor biopsies and UMSCC-1.
Conclusions: Combining bortezomib with cetuximab and radiation therapy showed unexpected early progression, evidence for EGFR stabilization, increased prosurvival signaling, and SCCHN cytokine expression, warranting avoidance of this combination. Clin Cancer Res; 17(17); 5755–64. ©2011 AACR.
PF-04691502, a Potent and Selective Oral Inhibitor of PI3K and mTOR Kinases with Antitumor Activity
Authors: Yuan Jing , Mehta Pramod P. , Yin Min-Jean , Sun Shaoxian , Zou Aihua , Chen Jeffrey , Rafidi Kristina , Feng Zheng , Nickel Jeffrey , Engebretsen Jon , Hallin Jill , Blasina Alessandra , Zhang Eric , Nguyen Leslie , Sun Minghao , Vogt Peter K. , McHarg Aileen , Cheng Hengmiao , Christensen James G. , Kan Julie L.C. , Bagrodia Shubha 
Published: July 2011

Abstract
Deregulation of the phosphoinositide 3-kinase (PI3K) signaling pathway such as by PTEN loss or PIK3CA mutation occurs frequently in human cancer and contributes to resistance to antitumor therapies. Inhibition of key signaling proteins in the pathway therefore represents a valuable targeting strategy for diverse cancers. PF-04691502 is an ATP-competitive PI3K/mTOR dual inhibitor, which potently inhibited recombinant class I PI3K and mTOR in biochemical assays and suppressed transformation of avian fibroblasts mediated by wild-type PI3K γ, δ, or mutant PI3Kα. In PIK3CA-mutant and PTEN-deleted cancer cell lines, PF-04691502 reduced phosphorylation of AKT T308 and AKT S473 (IC50 of 7.5–47 nmol/L and 3.8–20 nmol/L, respectively) and inhibited cell proliferation (IC50 of 179–313 nmol/L). PF-04691502 inhibited mTORC1 activity in cells as measured by PI3K-independent nutrient stimulated assay, with an IC50 of 32 nmol/L and inhibited the activation of PI3K and mTOR downstream effectors including AKT, FKHRL1, PRAS40, p70S6K, 4EBP1, and S6RP. Short-term exposure to PF-04691502 predominantly inhibited PI3K, whereas mTOR inhibition persisted for 24 to 48 hours. PF-04691502 induced cell cycle G1 arrest, concomitant with upregulation of p27 Kip1 and reduction of Rb. Antitumor activity was observed in U87 (PTEN null), SKOV3 (PIK3CA mutation), and gefitinib- and erlotinib-resistant non–small cell lung carcinoma xenografts. In summary, PF-04691502 is a potent dual PI3K/mTOR inhibitor with broad antitumor activity. PF-04691502 has entered phase I clinical trials. Mol Cancer Ther; 10(11); 2189–99. ©2011 AACR.
In VitroandIn VivoResponses of Advanced Prostate Tumors to PSMA ADC, an Auristatin-Conjugated Antibody to Prostate-Specific Membrane Antigen
Authors: Wang Xinning , Ma Dangshe , Olson William C. , Heston Warren D.W. 
Published: July 2011

AbstractProstate-specific membrane antigen (PSMA) is a membrane protein that is overexpressed manifold in prostate cancer and provides an attractive target for therapy. PSMA ADC is an antibody-drug conjugate (ADC) that consists of a fully human anti-PSMA monoclonal antibody conjugated to monomethylauristatin E through a valine-citrulline linker. In this study, the antitumor activity of PSMA ADC was evaluated against a panel of prostate cancer cell lines in vitro and in a novel in vivo model of taxane-refractory human prostate cancer. In vitro cell killing was efficient for cells with abundant PSMA expression (&gt;105 molecules/cell; IC50 ≤ 0.022 nmol/L) and 1,000-fold less efficient for cells with undetectable PSMA (IC50 &gt; 30 nmol/L). Intermediate potency (IC50 = 0.80 nmol/L) was observed for cells with approximately 104 molecules of PSMA per cell, indicating a threshold PSMA level for selective cell killing. Similar in vitro activity was observed against androgen-dependent and -independent cells that had abundant PSMA expression. In vitro activity of PSMA ADC was also dependent on internalization and proper N-glycosylation/folding of PSMA. In contrast, less potent and nonselective cytotoxic activity was observed for a control ADC, free monomethylauristatin E, and other microtubule inhibitors. PSMA ADC showed high in vivo activity in treating xenograft tumors that had progressed following an initial course of docetaxel therapy, including tumors that were large (&gt;700 mm3) before treatment with PSMA ADC. This study defines determinants of antitumor activity of a novel ADC. The findings here support the clinical evaluation of this agent in advanced prostate cancer. Mol Cancer Ther; 10(9); 1728–39. ©2011 AACR.
Convection-Driven Melting near the Grounding Lines of Ice Shelves and Tidewater Glaciers
Authors: Jenkins Adrian 
Published: July 2011

Abstract
Subglacial meltwater draining along the bed of fast-flowing, marine-terminating glaciers emerges at the grounding line, where the ice either goes afloat to form an ice shelf or terminates in a calving face. The input of freshwater to the ocean provides a source of buoyancy and drives convective motion alongside the ice–ocean interface. This process is modeled using the theory of buoyant plumes that has previously been applied to the study of the larger-scale circulation beneath ice shelves. The plume grows through entrainment of ocean waters, and the heat brought into the plume as a result drives melting at the ice–ocean interface. The equations are nondimensionalized by using scales appropriate for the region where the subglacial drainage, rather than the subsequent addition of meltwater, supplies the majority of the buoyancy forcing. It is found that the melt rate within this region can be approximated reasonably well by a function that is linear in ocean temperature, has a cube root dependence on the flux of subglacial meltwater, and has a complex dependency on the slope of the ice–ocean interface. The model is used to investigate variability in melting induced by changes in both ocean temperature and subglacial discharge for a number of realistic examples of ice shelves and tidewater glaciers. The results show how warming ocean waters and increasing subglacial drainage both generate increases in melting near the grounding line.
Comments on “The Depth-Dependent Current and Wave Interaction Equations: A Revision”
Authors: Bennis Anne-Claire , Ardhuin Fabrice 
Published: July 2011

Abstract
Equations for the wave-averaged three-dimensional momentum equations have been published in this journal. It appears that these equations are not consistent with the known depth-integrated momentum balance, especially over a sloping bottom. These equations should thus be considered with caution, because they can produce erroneous flows, particularly outside of the surf zone. It is suggested that the inconsistency in the equations may arise from the different averaging operators applied to the different terms of the momentum equation. It is concluded that other forms of the momentum equations, expressed in terms of the quasi-Eulerian velocity, are better suited for three-dimensional modeling of wave–current interactions.
JAK2V617F mutation and hydroxyurea treatment as determinants of immature platelet parameters in essential thrombocythemia and polycythemia vera patients
Authors: Panova-Noeva Marina , Marchetti Marina , Buoro Sabrina , Russo Laura , Leuzzi Annamaria , Finazzi Guido , Rambaldi Alessandro , Ottomano Cosimo , ten Cate Hugo , Falanga Anna 
Published: July 2011

Abstract
Immature platelets (IPFs), which are hemostatically more active than mature platelets, have been found elevated in essential thrombocythemia and polycythemia vera, 2 myeloproliferative neoplasms (MPN) characterized by an increased risk of thrombosis. It is not known whether the IPF levels are influenced by pathogenetic factors, including JAK2V617F mutational status, or by treatment regimen. To address this point, in 46 essential thrombocythemia and 38 polycythemia vera consecutive patients, we measured IPF and correlated the results to JAK2V617F mutation and myelosuppressive treatment with hydroxyurea. This analysis provides 2 new elements regarding IPF and MPN. The first finding is that the JAK2V617F mutation is linked to the quantity of IPF in patients with MPN, which might contribute to the prothrombotic phenotype in these patients. The second finding is that IPF is susceptible to myelosuppressive treatment, which may additionally explain the favorable effect of hydroxyurea therapy on MPN outcome as well as the associated thrombotic risk.
Reduction in plasma cell proliferation after initial therapy in newly diagnosed multiple myeloma measures treatment response and predicts improved survival
Authors: Larsen Jeremy T. , Chee Cheng E. , Lust John A. , Greipp Philip R. , Rajkumar S. Vincent 
Published: July 2011

Abstract
Standard myeloma treatment response criteria are determined principally by changes in the monoclonal protein. Reduction in the size of the proliferative component of malignant plasma cells may be an additional metric of assessing response to therapy. We retrospectively analyzed 176 patients with newly diagnosed myeloma with a measurable plasma cell labeling index (PCLI) at diagnosis and repeat measurement 4 months after initiation of therapy. PCLI response was defined as a ≥ 60% reduction. Baseline PCLI is an independent prognostic factor; therefore, we categorized patients into 3 groups: PCLI ≥ 3% (high), ≥ 1% (intermediate), and < 1% (low). Patients achieving a greater PCLI response had improved median overall survival of 54 months compared with 29 months in nonresponders (P = .02). Improved median overall survival with PCLI response occurred in the high initial PCLI group (28 vs 7 months; P = .003) and intermediate group (64 vs 24 months; P = .002). The application of PCLI response and serum M-spike response together provided further prognostic information. On multivariate analysis, the prognostic value of PCLI response was independent of β2-microglobulin, elevated creatinine, serum M-spike response, and baseline PCLI. We conclude that a significant reduction in plasma cell proliferation in patients with newly diagnosed myeloma is an important predictor of survival.
Health-related quality of life in chronic myeloid leukemia patients receiving long-term therapy with imatinib compared with the general population
Authors: Efficace Fabio , Baccarani Michele , Breccia Massimo , Alimena Giuliana , Rosti Gianantonio , Cottone Francesco , Deliliers Giorgio Lambertenghi , Baratè Claudia , Rossi Antonella Russo , Fioritoni Giuseppe , Luciano Luigia , Turri Diamante , Martino Bruno , Di Raimondo Francesco , Dabusti Melissa , Bergamaschi Micaela , Leoni Pietro , Simula Maria Pina , Levato Luciano , Ulisciani Stefano , Veneri Dino , Sica Simona , Rambaldi Alessandro , Vignetti Marco , Mandelli Franco ,   for GIMEMA
Published: July 2011

Abstract
The main objective of this study was to investigate whether patients with chronic myeloid leukemia (CML) in treatment with long-term therapy imatinib have a different health-related quality-of-life (HRQOL) profile compared with the general population. In total, 448 CML patients were enrolled, and the SF-36 Health Survey was used to compare generic HRQOL profiles. Symptoms were also assessed. HRQOL comparisons were adjusted for key possible confounders. The median age of patients was 57 years and the median time of imatinib treatment was 5 years (range 3-9 years). The largest HRQOL differences were found in younger patients. In particular, patients aged between 18 and 39 years had marked impairments in role limitations because of physical and emotional problems, respectively: −22.6 (P < .001), −22.3 (P < .001). Patients with CML age 60 or older had a HRQOL profile very similar to that reported by the general population. Women had a worse profile than men when each were compared with their peers in the general population. Fatigue was the most frequently reported symptom. The HRQOL of CML patients is comparable with that of population norms in many areas, however, younger and female patients seem to report the major limitations.
Differential modulation of cytokine, chemokine and Toll like receptor expression in chickens infected with classical and variant infectious bursal disease virus
Authors: Rauf Abdul , Khatri Mahesh , Murgia Maria V , Jung Kwonil , Saif Yehia M 
Published: July 2011

AbstractInfectious bursal disease (IBD) is an important immunosuppressive disease of chickens. The causative agent, infectious bursal disease virus (IBDV), consists of two serotypes, 1 and 2. Serotype 1 consists of classic IBDV (cIBDV) and variant IBDV (vIBDV). Both of these strains vary in antigenicity and pathogenesis. The goal of this study was to compare the immunopathogenesis of cIBDV and vIBDV. Three-week-old specific pathogen free chickens were inoculated intraocularly with standard challenge strain (STC) (cIBDV) and a variant strain Indiana (IN) (vIBDV). The cIBDV produced more pronounced bursal damage, inflammatory response and infiltration of T cells as compared to vIBDV. There were significant differences in the expression of innate (IFN-α and IFN-β), proinflammatory cytokine and mediator (IL-6 and iNOS) in cIBDV- and vIBDV-infected bursas. The expression of chemokines genes, IL-8 and MIP-α was also higher in cIBDV-infected chickens during the early phase of infection. The expression of Toll like receptor 3 (TLR3) was downregulated at post inoculation days (PIDs) 3, 5, and 7 in the bursas of vIBDV-infected chickens whereas TLR3 was upregulated at PIDs 3 and 5 in cIBDV-infected bursas. In vIBDV-infected bursa, TLR7 expression was downregulated at PIDs 3 and 5 and upregulated at PID 7. However, TLR7 was upregulated at PIDs 3 and 7 in cIBDV-infected bursas. The expression of MyD88 was downregulated whereas TRIF gene expression was upregulated in cIBDV- and vIBDV-infected bursa. These findings demonstrate the critical differences in bursal lesions, infiltration of T cells, expression of cytokines, chemokines and TLRs in the bursa of cIBDV-and vIBDV-infected chickens.