tbuckley/cabot-search huggingface dataset:
OP0195-HPR Nurse-led rheumatology clinic versus rheumatologist clinic in monitoring of biological therapy– a randomised controlled study:
Authors: I. Larsson, B. Arvidsson, B. Fridlund, A. Teleman, S. Bergman
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Patients with rheumatic diseases treated with biological therapy are usually followed up by rheumatologists. Nurse-led rheumatology clinics have been proposed for patients with low disease activity or in remission. <h3>Objectives</h3> To compare treatment outcomes from a nurse-led rheumatology clinic and a rheumatologist clinic for patients treated with biological therapy with low disease activity or in remission. <h3>Methods</h3> In a prospective controlled study 107 patients were randomised into two groups with six months follow up to a nurse-led rheumatology clinic (intervention group; n=53) or to a rheumatologist clinic (control group; n=54). Inclusion criteria were ongoing biological therapy and Disease Activity Score 28 (DAS28) ≤3.2. All patients met the rheumatologist at inclusion and after 12 months. In the nurse-led rheumatology clinic the patients’ disease activity was assessed by examination of tender or swollen joints and laboratory tests. The rheumatology nurse also had a dialogue concerning the patient’s needs with regard to drug therapy, smoking habits and psychosocial aspects. Main outcome was disease activity measured by DAS28. <h3>Results</h3> After 12 months 97 patients completed the study. The patients had mean age of 55.4 years, disease duration of 16.7 years, and DAS28 was 2.1, with no significant differences between the two groups. In change of DAS28 there were no differences (p=0.66) between the intervention group (0.14) or control group (0.20) from inclusion to 12 months. There were no differences (p&gt;0.05) in mean change after 12 months in ESR, swollen and tender joints, global health and pain visual analogue scales (VAS) or Health Assessment Questionnaire (HAQ) between the patients followed up at the nurse-led rheumatology clinic or the rheumatologist clinic, see table. <h3>Conclusions</h3> Patients with low disease activity or in remission, in biological therapy could be monitored by a nurse-led rheumatology clinic without any differences in outcome as measured by DAS28. <h3>Disclosure of Interest</h3> None Declared
Abstract 4754: A humanized, high affinity anti-CCR4 antibody for immunotherapy of cutaneous T cell lymphoma and characterization on T cell function.
Authors: DeKuan Chang, Thomas Han, Rachael A. Clark, Quan Zhu, Thomas S. Kupper, Wayne A. Marasco
Journal: Cancer Research (2013)

Abstract Cutaneous T-cell lymphoma (CTCL) is a heterogeneous group of neoplastic disorders characterized by clonally derived and skin-homing malignant T cells that express high level of chemokine receptor CCR4, which is associated with their skin-homing capacity. CCR4 is also highly expressed on T-regulatory cells (Tregs) that can migrate to several different types of chemotactic ligand CCL17- and CCL22-secreting tumors to facilitate tumor cell evasion from immune surveillance. Thus, its high-level expression on CTCL cells and Tregs makes CCR4 a potential ideal target for antibody-based immunotherapy for CTCL and other types of solid tumors. Here, a humanized and affinity optimized anti-CCR4 monoclonal antibody (mAb), mAb2-3, was evaluated. In vitro mechanism studies demonstrated that the potent in vivo anti-tumor effects of this humanized anti-CCR4 mAb could be attributed to antibody dependent cellular cytotoxicity (ADCC), complement mediated cytotoxicity (CDC) and antibody dependent cellular phagocytosis (ADCP). In a mouse CTCL tumor model, anti-CCR4 mAb exhibited an antitumor effect by mediating cellular cytotoxicity through CDC and ADCC via FcγRIIIa expressed murine neutrophils and human nature killer (NK) cells. Moreover, this anti-CCR4 mAb also effectively inhibits chemotaxis of CD4+CD25high Tregs via CCL22 and abrogates Treg suppression activity in vitro by restoring the proliferation of CD4+CD25− effector T cells (Teffs). Taken together, this high-affinity humanized mAb2-3 with potent antitumor effect and a broad range of mechanisms of action on immunity may provide a novel immunotherapy for CTCL and other solid tumors. Citation Format: DeKuan Chang, Thomas Han, Rachael A. Clark, Quan Zhu, Thomas S. Kupper, Wayne A. Marasco. A humanized, high affinity anti-CCR4 antibody for immunotherapy of cutaneous T cell lymphoma and characterization on T cell function. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4754. doi:10.1158/1538-7445.AM2013-4754
Abstract 1515: Epigenetic silencing of retinoblastoma gene regulates pathologic differentiation of myeloid cells in cancer.
Authors: Je-In Youn, Vinit Kumar, Michelle Collazo, Dmitry I. Gabrilovich
Journal: Cancer Research (2013)

Abstract Myeloid-derived suppressor cells (MDSC) are one of the major factors negatively regulating immune responses in cancer and many other pathologic conditions. These cells consist of two distinct populations: monocytic MDSC (M-MDSC) and polymorphonuclear MDSC (PMN-MDSC). PMN-MDSC is the predominant group of MDSC accumulated in cancer. Under physiologic conditions, the normal counterpart of M-MDSC - Ly6ChiLy6G- inflammatory monocytes (Mon) differentiate in periphery tissues to macrophages (MΦ) and dendritic cells (DCs). In contrast, a large proportion of M-MDSC, in tumor-bearing mice, acquired phenotypic, morphological and functional features of PMN-MDSC. In human, CD14+HLA-DR-/low M-MDSC from patients with multiple myeloma also differentiated into CD66b+ PMN-MDSC. This effect was caused by soluble tumor-derived factors and mediated by transcriptional silencing of the retinoblastoma (Rb) gene. M-MDSC had an amount of Rb1 similar to that in mature myeloid cells (PMN, DCs) while Rb1 was barely detectable in PMN-MDSC. Lack of Rb1 in mice with conditional deletion of the gene promoted an expansion of splenic CD11b+Ly6G+Ly6Clo cells, similar to the phenotype of PMN-MDSC in tumor-bearing mice. Moreover, immunogeneic EG7 tumor grew much faster in Rb1-KO mice than in Rb1-WT littermates. Mon from Rb1-KO mice acquired significantly increased proportion of PMN after in vitro culture compared to Rb1-WT Mon. In contrast, the overexpression of Rb1 substantially reduced the proportion of PMN-MDSC differentiated from M-MDSC. Histone deacetylase 2 (HDAC-2) was directly involved in down-regulation of Rb1 expression. Inhibition of HDAC in MDSC resulted in the increase in their Rb1 expression, abrogated differentiation of M-MDSC to PMN-MDSC, and restored M-MDSC differentiation towards DCs and MΦ. These results suggest that down-regulation of Rb by epigenetic modification plays a major role in accumulation of MDSC in cancer by regulating PMN-MDSC differentiation from M-MDSC. HDAC may be considered as potential targets for therapeutic regulation of MDSC in cancer. Citation Format: Je-In Youn, Vinit Kumar, Michelle Collazo, Dmitry I. Gabrilovich. Epigenetic silencing of retinoblastoma gene regulates pathologic differentiation of myeloid cells in cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1515. doi:10.1158/1538-7445.AM2013-1515 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
Tc-99m RBC SPECT Showing Colonic Bleeding in Traumatic Pseudoaneurysm with Arteriocolonic Fistula
Authors: JONG-KANG LEE, WEI-JEN SHIH, CHIN-MIN CHUANG
Journal: Clinical Nuclear Medicine (1998)

Splanchnic artery pseudoaneurysms are rare but life-threatening vascular lesions. Rupture or leakage of the pseudoaneurysm often produces gastrointestinal bleeding if the pseudoaneurysm is in connection with the gastrointestinal lumen. Presented is the case of a patient with a traumatic pseudoaneurysm of one of the branches of the superior mesenteric artery as an arterioenteric fistula with massive gastrointestinal bleeding. Abdominal Tc-99m labeled RBC scintigraphy and abdominal SPECT images accurately identified the source of the gastrointestinal bleeding as an arterioenteric fistula secondary to a pseudoaneurysm of one of the branches of the superior mesenteric artery, thereby facilitating prompt surgical repair.
Treatment of intermittent intussusception in Peutz–Jeghers syndrome with single-balloon enteroscopy
Authors: J.-H. Lai, C.-W. Chang, M.-J. Chen, S.-C. Lin, H.-Y. Wang, C.-W. Chang
Journal: Endoscopy (2010)

A 30-year-old woman with Peutz–Jeghers syndrome (PJS) had a known history of jejunal intussusception with partial resection of the jejunum 7 years previously. The PJS was under surveillance with regular polypectomy by colonoscopy every year in our hospital. She attended our department again with a 1 month history of intermittent upper abdominal cramping pain and bile-like vomitus. Single-balloon enteroscopy (SBE) showed transient intussusception in the proximal jejunum which was caused by a 3-cm broad-based polyp ([Fig. 1]).
Abstract 3476: Blockade of endothelial Notch diminishes tumor growth and perfusion
Authors: Alexandre Patenaude, Linda Chang, Erika Diaz, Megan Fuller, Fred Wong, Aly Karsan
Journal: Cancer Research (2011)

Abstract Canonical Notch signaling comprises a family of receptors and ligands that modulate cell fate and differentiation. Upon ligand binding, Notch receptors undergo a series of cleavages that culminate in the translocation of the intracellular domain to the nucleus, resulting in transcriptional activation through the derepression and activation at CSL-bound promoters. Notch activity is essential for embryonic vascular development and was recently also shown to be important for adult neovascularization. Notably, blocking Notch signaling by inhibition of the ligand Dll4 increased endothelial proliferation and sprouting, but resulted in non-perfused vasculature and tumor growth inhibition. Moreover, Dll4 inhibition was shown to diminish vascular mural cells, such as pericytes, in tumors. Whether these effects of Dll4 blockade on tumor vasculature resulted specifically from Notch inhibition in endothelial cells remains to be fully elucidated. We investigated this question using a tetracycline-inducible binary transgenic system, in which Notch is blocked by the expression of a dominant-negative form of mastermind-like 1 (dnMAML-GFP) under the control of the VE-cadherin promoter. Lewis lung carcinoma (LLC) cells overexpressing VEGFA (LLC-VEGFA) were implanted subcutaneously in the dorsa of double transgenic (Tg) or control mice. Tumors in the double Tg mice were significantly smaller than in control single Tg mice. Moreover, blood vessel perfusion from LLC-VEGFA tumors was significantly reduced in the double Tg mice compared to the control Tg mice. However, neither the abundance nor the branching architecture of LLC-VEGFA tumor blood vessels appeared to be different in the double Tg mice. Pericyte abundance, maturation and distribution relative to blood vessels did not change in the double Tg mice. Flow cytometry of tumor-derived cells and fluorescence microscopy analysis of tumor cryosections confirmed that dnMAML-GFP is expressed specifically in endothelial cells. Our data suggest that specific blockade of Notch in endothelial cells, induced by dnMAML-GFP, affects tumor growth through a mechanism different from previously-reported Dll4 inhibition studies. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3476. doi:10.1158/1538-7445.AM2011-3476
A6.19 Identification of an unexpected dysregulated pathway by transcriptomic analysis of monocyte-derived dendritic cells (MD-DCS) in spondyloarthritis (SPA) patients
Authors: C Desjardin, C Hue, S Grassin-Delyle, H-J Garchon, E Chaplais, M Breban, G Chiocchia
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> Spondyloarthritis (SpA) is one of the most frequent chronic inflammatory rheumatisms that affects axial skeleton, peripheral joints and may result in ankylosis of the spine and sacroiliac joints. Extra-articular features including uveitis, psoriasis and inflammatory bowel disease are frequent. Current SpA treatments are only symptomatic, relieving inflammatory symptoms. SpA aetiology is largely multifactorial with a genetic component dominated by the association with the HLA-B27 allele. This allele, however, is not sufficient for the disease to occur. Whereas dendritic cells (DCs) are believed to play a key role in SpA pathogenesis, the precise mechanisms underlying disease development and the role of HLA-B27 remain poorly understood. To shed light on the genes involved, we recently carried out a transcriptomic analysis of monocyte-derived DCs (MD-DCs) from patients and healthy controls, also accounting for HLA-B27. <h3>Material and methods</h3> Transcriptomic profiles of MD-DCs were obtained with the Affymetrix Human Gene 1.0 ST technology from SpA patients (n = 23 HLA-B27+) and from healthy controls (n = 23 HLA-B27+, n = 21 HLA-B27-). Analysis of differentially expressed (DE) genes was conducted with LIMMA accounting for both the disease and the HLA-B27 status, followed by quantitative gene set enrichment analyses (quSAGE) and functional annotation. We performed three comparisons to identify DE genes and generating three lists: A, including 800 DE genes between SpA patients and HLA-B27- controls; B, including 673 DE genes between HLA-B27+ controls and HLA-B27- controls; and C, including 466 DE genes between SpA patients and HLA-B27+ controls. Subtracting A–B left 656 genes, of which 68 are in list C. <h3>Results</h3> By combining a transcriptomic analysis and innovative comparative approaches, we identified a set of 68 genes affected by SpA overcoming the potential HLA-B27 effect. Based on functional annotation, those genes are mainly related to lipid synthesis, regulation and trafficking suggesting that MD-DCs from SpA patients exhibit major functional dysregulations. <h3>Conclusion</h3> In SpA patients, DCs present a defect in lipid intracellular regulation and signalling which may be involved in SpA physiopathology and may contribute to its development and progression. Our work may help to improve the understanding of SpA pathogenesis and open new perspectives in therapeutic approaches.
P4-14-05: Chemotherapy-Induced Alopecia, Body Image and Psychological Distress in Women with Breast Cancer: A Prospective Study.
Authors: E-K Choi, I-R Kim, S-J Nam, J Lee, J Yang, S-K Lee, D-Y Noh, W Han, J Cho
Journal: Cancer Research (2011)

Abstract Purpose: While chemotherapy-induced alopecia (CIA) is known to be associated with lower quality of life, the longitudinal effect of alopecia on body image and distress in unknown. This study examined effect of CIA on body image and psychological distress during active breast cancer treatment. Patients and Methods Between July and Dec 2010, we recruited patients with non-metastatic breast cancer who were expected to receive adjuvant chemotherapy (N=411) from two cancer hospitals in Seoul, Korea. After excluding 15 patients with recurrence and 65 patients lost to follow-up, the present analysis is based on 331 patients (80.5%). Participants completed questionnaires on body image, quality of life, alopecia distress at enrollment (before surgery), before chemotherapy (2 weeks post surgery), during chemotherapy (3 months post surgery), and after chemotherapy (6 months post surgery). Body image and quality of life were assessed by the EORTC QoL Questionnaire BR23. Alopecia distress was assessed by the Alopecia Distress Scale, which evaluated distress in 4 domains: physical, emotional, daily activity, and relationship. Results: The mean age of the participants was 46.4 (SD 7.91) year. 44.9% and 37.6% of them had stage I and II breast cancer, respectively. 83.0% of the patients had lumpectomy, and 70.6% and 85.9% had chemotherapy and radiotherapy, respectively. Patients who experienced alopecia had a significantly more negative body image and higher distress compared to those who did not experience alopecia. Body image rapidly decreased at 3 months post surgery coinciding with alopecia, and its effects lasted until 6 months post surgery. Moreover, there was a highly statistically significant association between more negative body image and higher alopecia distress after adjusting for other socio-demographic and clinical characteristics. The patterns and changes in body image and distress comparing patients with and without alopecia are reported in Table 1. Discussion: Health professionals need to develop clinical pathways and education programs to help women with breast cancer manage alopecia distress and negative body image during active treatment. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P4-14-05.
Abstract P6-05-05: Signaling Pathways Activated in Her 2 and ER Negative Breast Cancers
Authors: D Song, L Gao, M Cui, B Han, G Zhao, T Fu, P Li, F Ye, MZ Fan, G Pelletier, DY. Zhang
Journal: Cancer Research (2010)

Abstract Introduction: Breast cancer is the most common cancer in women (192,370 new cases in 2009) and the second leading cause of cancer death (40,000) among women in USA. Current multimodality treatment of breast cancer is based on the level of ER expression and Her 2 gene amplification. However, no effective treatment is currently available for breast cancers with low level expression of ER and no amplification of Her 2 gene. The aim of this study is to identify protein pathways activated in the breast cancer with negative expression of ER and Her 2. Method: Protein Pathway Array was used to assess the level of protein expression and phosphorylation in 71 paired fresh frozen breast samples (tumor and adjacent benign tissue). A total 159 antibodies were evaluated which represent most important signal transduction pathways involved in proliferation, apoptosis, angiogenesis, invasion and metastasis. Several potential therapeutic kinase proteins were also assessed. Results: A total 20 proteins (PCNA, phospho-PTEN, cyclin B1 cyclin E1, CDK6, E-cadherin, NFkB, ect) were differentially expressed between normal and tumor tissues based on the statistical analysis. In Her 2 negative tumors (n=37), 3 proteins were differentially expressed and among them, 2 were up-regulated (CDK6 and HSD1) and 1 was down-regulated (IGF). In ER negative tumors (n=18), 4 proteins (HSD, SK, TDP and Slug) was up-regulated and 1 proteins were down-regulated (E-cadherin). In triple negative tumors (n=13), one protein (E-cadherin) down-regulated and 2 proteins (TDP and HSD) were up-regulated. Furthermore, based on the expression pattern of these proteins, tumors negative for both ER and Her 2 (n=15) can be clustered into 3 groups Figure 1: Subclassification of breast cancers negative for ER and Her-2 based protein pattern. Hierarchical clustering analysis of 20 differentially expressed proteins in 15 ER/Her-2 negative breast cancers. The cancers can be separated into 3 subtypes. Red indicates overexpression, green underexpression, black no change, and gray no expression. Each column represents a protein. Each row represents a sample. Conclusion: Our study showed that distinct sets of signaling pathways activated in ER and Her 2 negative breast cancers. The increased expression of cell cycle progression proteins in Her 2 negative tumors suggests activation of cell proliferation via different growth promotion pathway. Similarly, different cell proliferation pathways are also activated in ER negative tumors. This finding may be used to design future clinical trial based on the activation of different signaling pathways. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P6-05-05.
[MMA:DMA Ratios Reversed]: Response
Authors: Paul Mushak
Journal: Environmental Health Perspectives (1997)

s Focus article, "Measuring Mercury" (1), which appeared in the August 1996 issue of EHP, contained a serious omission.Wheeler concentrated on methyl mercury and, to a lesser extent, ele- mental mercury in dental amalgams.He failed to mention the relatively recently described but extremely significant expo- sures to elemental mercury in ethnically Hispanic and Caribbean homes, conse- quent to its use for a variety of magico-religious and ethnomedical purposes (2-3).Such domestic use and presumed expo- sure has been documented in a number of published papers, as well as by research sponsored by the ATSDR (4-6) and the EPA (7).In fact, an ATSDR monograph specifically alerts clinicians to this exposure pathway: "Metallic mercury has been used by Mexican-Americans and Asian popula- tions in folk remedies for chronic stomach disorders and by Latin-American and Caribbean natives in occult practices" (4).This monograph was edited by Thomas Clarkson, who was interviewed by Wheeler, and who has long been aware of elemental mercury's domestic use.Similarly, the EPA's Kathryn Mahaffey, also interviewed, has been aware of domestic mercury exposure for some years, and the EPA issued a risk assessment document on cultural uses of mercury in 1993 (7).These mercury exposures are especially significant from an environmental health perspective because, in many cases, they are certain to be orders of magnitude greater than (methyl) mercury exposures from eating fish or from the leaching of mercury in amalgam fillings.Additionally, the mercury vapor released from mercury intentionally sprinkled on floors affects all occupants of contaminated homes, from the fetus to the elderly.Andrew Rowland, cited in "The Issue of Amalgams" (1), has been aware of domestic mercury exposure for several years.Rowland makes a call for more research on health effects of amalgam-mercury exposure.I make a similar call for research on magico-religious mercury exposure.If the environmental health research community continues to ignore magico-religious mercury exposure, its health effects will never be ascertained.
943 PROSPECTIVE MAGNETIC RESONANCE CHOLANGIOGRAM STUDY TO DEFINE THE PREVALENCE AND CHARACTERISTICS OF PRIMARY SCLEROSING CHOLANGITIS IN PATIENTS WITH ULCERATIVE COLITIS AND COLORECTAL DYSPLASIA
Authors: E.L. Culver, H.K. Bungay, J.R.F. Cummings, M. Betts, B.F. Warren, D. Delaney, S.P. Travis, E. Barnes, R.W. Chapman
Journal: Journal of Hepatology (2012)
Limited human-to-human transmission of avian influenza A(H7N9) virus, Shanghai, China, March to April 2013
Authors: J Hu, Y Zhu, B Zhao, J Li, L Liu, K Gu, W Zhang, H Su, Z Teng, S Tang, Z Yuan, Z Feng, F Wu
Journal: Eurosurveillance (2014)

In April 2013, two members of one family were successively confirmed as cases of avian influenza A(H7N9) virus infection in Shanghai, China. Respiratory specimens from the two cases and their close contacts were tested using real-time reverse-transcription (RT)-PCR. Paired serum specimens from contacts were tested by haemagglutination inhibition assay and microneutralisation test. The index patient developed severe pneumonia. Her husband presented with pneumonia shortly thereafter. Both cases had highly similar clinical features and infection with A(H7N9) virus was confirmed in both cases by genetic analysis. Phylogenetic analysis revealed a high level of similarity between the sequences from the two patients and environmental samples collected from wet markets in Minhang and Changning districts. Six samples from the Changning wet market were confirmed as A(H7N9) positive. Of 27 close contacts, one developed mild respiratory symptoms and another tested positive for A(H7N9) antibodies, but both were negative by real-time RT-PCR. The other 25 close contacts of both cases were A(H7N9) negative. Limited human-to-human transmission of the virus most likely occurred in the family cluster. However, other close contacts did not test positive for the virus, suggesting limited potential for extensive human-to-human transmission of the virus.