tbuckley/cabot-search huggingface dataset:
Difference in Endoscopic Ultrasound's diagnostic accuracy of vascular involvement between different vessels in pancreatic cancer
Authors: S Puli, S Singh, J Talapaneni, M Oropeza-vail, M Olyaee
Journal: Endoscopy (2006)

Introduction: The difference in accuracy for vascular invasion (VI) between portal vein and superior mesenteric (SM) vessels in patients with pancreatic cancer has not been well studied. Goal: To asses difference in accuracy of EUS to diagnose vascular invasion or adherence between portal vein and superior mesenteric vessels. Method: Patients who had pre-operative EUS and subsequently underwent surgery were identified in a retrospective manner. EUS criteria for vascular adhesion was loss of echoplane alone. Vascular invasion was defined as tumor in the lumen, abnormal vessel contour, the presence of collateral vessels in the absence of a main vascular structure. Surgical definition for vascular adhesion was – tumor adherence but resectable and vascular invasion was defined as tumor encasing the vessel or vascular unresectability. Results: Total of 77 patients with pancreatic cancer and VI were identified. 41 patients had surgery at our institution. EUS showed vascular involvement in 25 patients and no involvement in 16 patients. The accuracy of EUS for vascular invasion and vascular adhesion between portal vein and superior mesenteric vessels is shown in table 1.
SPONTANEOUS IMMUNE RESPONSES IN GBM PATIENTS AFTER COMPLETE TUMOR RESECTION ARE ASSOCIATED WITH AN IMPROVED SURVIVAL
Authors: C. Herold-Mende, J. Mossemann, C. Jungk, R. Ahmadi, D. Capper, A. von Deimling, A. Unterberg, P. Beckhove
Journal: Neuro-Oncology (2014)

BACKGROUND: Spontaneous anti-tumor immune responses have been detected in several tumor types. However, not only in glioblastoma it is unclear if such immune responses influence patient outcome. METHODS: To detect such immune responses, occurence and frequencies of memory T-cells were determined in the peripheral blood of GBM patients applying the IFN gamma ELISPOT assay and using corresponding tumor lysates (n = 106) or a set of immunogenic polypeptides (n = 32). Extent of resection was assessed by either intraoperative or early postoperative MRI. In addition, intratumoral infiltration of different T-cell subpopulations at the time of first diagnosis was analyzed by immunohistochemistry (n = 20) and compared to the occurrence of spontaneous immune responses. RESULTS: Altogether, T-cell responses against autologous tumor lysate were detected in 61/106 patients. Subsequent survival analysis concentrating on IDH1wt glioblastoma revealed a significant difference towards an improved survival for patients with a spontaneous immune response (p = 0.0251). Most interestingly, when stratifying for the extent of surgery those patients, who got a complete tumor resection and showed a spontaneous T cell response, survived significantly longer (p = 0.0002). In contrast, in subtotally resected patients the immune response did not improve survival. In line with these observations, occurrence of memory T cell responses against a set of known GBM-associated antigens (TTR, MAGE A3, S100A9) also trended to a better survival in those GBM patients who responded to all three antigens (p = 0.0663). Finally, increased frequency of intratumoral T cell infiltrates was also associated with the occurrence of spontaneous immune responses and an improved survival (p = 0.0113). CONCLUSIONS: The present analysis for the first time depicts on several levels a significant influence of the patient's immune system on the course of the disease in GBM patients. In this regard the most crucial prerequisite seems to be the MRI-based complete tumor resection. Most likely surgical removal of the immunosuppressive tumor environment allows for the beneficial reactivation of pre-existing immune responses. SECONDARY CATEGORY: Tumor Biology.
GLOBAL LONGITUDINAL STRAIN BY 3D SPECKLE TRACKING AFTER ST-ELEVATION MYOCARDIAL INFARCTION IS USEFUL FOR PREDICTING LEFT VENTRICULAR REMODELING: COMPARISON WITH TC99M-SESTAMIBI
Authors: Noriaki Iwahashi, Masaomi Gohbara, Shunsuke Kataoka, Eiichi Akiyama, Nobuhiko Maejima, Kengo Tsukahara, Kiyoshi Hibi, Masami Kosuge, Toshiaki Ebina, Satoshi Umemura, Kazuo Kimura
Journal: Journal of the American College of Cardiology (2015)
GENETIC AND HISTOLOGICAL STABILITY OF OLIGODENDROGLIAL TUMORS WITH 1P/19Q CO-DELETION EVEN AFTER CHEMOTHERAPY AND OR RADIATION THERAPY
Authors: K. Ueki, K. Aihara, A. Mukasa, F. Higuchi, H. Matsuda, P. Kim
Journal: Neuro-Oncology (2014)

BACKGROUND: Among number of genetic markers in gliomas, 1p/19q co-deletion in grade 2-3 gliomas is the most established marker in predicting chemosensitivity and surprisingly better prognosis. The mechanism for such distinct clinical features is not well understood. METHODS: We have retrospectively analyzed the treatment result of 1p/19q codeleted gliomas to elucidate the mechanism underlying such clinical features. For recurrent tumors that were resected, genetic and histological examinations were performed to see the changes in the recurrent tumors. RESULTS: Of 31 gliomas with 1p/19q co-deletion, 5 were not given any adjuvant therapy, 18 were treated with chemotherapy alone, and 7 underwent radiation therapy with chemotherapy. With the median follow-up of 48 months, 12 out of the 31 recurred, but the histological grades remained to be 2 or 3, showing slow growth, and responded to additional therapy well. In 9 cases, genetic testing for 1p/19q, 10q loss was peformed in recurrent tumors, and the alterations remained the same without additional 10q loss, the hallmark of grade 4 gliomas (glioblastoma). Copy number alterations of whole genome was also examined in selected cases, that also showed fewer additional genetic changes compared to the previous studies on astrocytic tumors. CONCLUSIONS: Thus, slow growth and relative genetic stability after genotoxic treatment may be the feature of those gliomas leading to the better prognosis compared to the rest. SECONDARY CATEGORY: Clinical Neuro-Oncology.
1186 ITPA GENE VARIANTS PREDICT HEMOLYTIC RIBAVIRIN INDUCED ANAEMIA IN PATIENTS TREATED WITH THE INTERFERON-FREE REGIMEN OF FALDAPREVIR, BI 207127 AND RIBAVIRIN IN SOUND-C2
Authors: T. Asselah, S. Zeuzem, V. Soriano, J.-P. Bronowicki, A.W. Lohse, B. Müllhaupt, M. Schuchmann, M. Bourliere, M. Buti, S. Roberts, E. Gane, J.O. Stern, F. Voss, P. Baum, J.-P. Gallivan, W.O. Böcher, F.J. Mensa
Journal: Journal of Hepatology (2013)
Abstract 586: Genomic and functional characterizations of phosphodiesterase 4Din human cancers.
Authors: Dechen Lin, Liang Xu, Ling-Wen Ding, Arjun Sharma, Li-Zhen Liu, Henry Yang, Patrick Tan, Jay Vadgama, Beth Karlan, Jenny Lester, Nicole Urban, Michèl Schummer, Ngan Doan, Jonathan Said, Martin Walsh, Paresma Patel, Craig Thomas, Daniel Chan, Phillip Koeffler
Journal: Cancer Research (2013)

Abstract Background Phosphodiesterase 4D (PDE4D) degrades the secondary messenger adenosine 3’, 5’-cyclic monophosphate (cAMP). PDE4D recently was implicated in cancer cell proliferation, but alterations in its genome and function in tumors are unclear. Methods PDE4D gene copy number determined by SNP-CHIP was comprehensively analyzed in a large number of solid tumor specimens from diverse origins (n=5,569). Expression of PDE4D gene transcripts were examined in 971 primary tumors, as well as established cancer cell lines. PDE4D protein expression in 11 different types of cancers were evaluated by immunohistochemistry (n=165). Endogenous PDE4D in multiple types of tumor cell lines was suppressed by both shRNAs and compound 26B, a novel inhibitor of PDE4D, and the effects on apoptosis and proliferation were examined. We further investigated the molecular mechanisms involved. Effect of ectopic expression of PDE4D on tumor growth was assessed both in vitro and in vivo. Results Homozygous deletion of PDE4D occurred in 198 cases out of 5,569 primary solid tumors (3.56%), with most of them being internal microdeletions. Unexpectedly, these internal microdeletions did not result in loss of its gene products, as the expression of PDE4D mRNA and protein was not compromised in the PDE4D-microdeleted samples. Immunohistochemistry staining revealed that PDE4D protein levels were up-regulated in several types of tumors. Importantly, genetic and pharmacological suppression of endogenous PDE4D caused apoptosis and growth inhibition preferentially in a variety of cancer cells but not in non-malignant epithelial cells. We further showed that anti-tumor events triggered by PDE4D-suppression were lineage-dependently associated with induction of BIM and down-regulation of MITF. Moreover, ectopic expression of the PDE4D short isoform (PDE4D2) enhanced the proliferation of melanoma both in vitro and in vivo. Conclusions We show for the first time that although targeted by genomic homozygous microdeletions, alternatively spliced PDE4D can function as a tumor-promoting factor. PDE4D represents a novel, targetable enzyme of cancer cells. Citation Format: Dechen Lin, Liang Xu, Ling-Wen Ding, Arjun Sharma, Li-Zhen Liu, Henry Yang, Patrick Tan, Jay Vadgama, Beth Karlan, Jenny Lester, Nicole Urban, Michèl Schummer, Ngan Doan, Jonathan Said, Martin Walsh, Paresma Patel, Craig Thomas, Daniel Chan, Phillip Koeffler. Genomic and functional characterizations of phosphodiesterase 4Din human cancers. [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 586. doi:10.1158/1538-7445.AM2013-586
Guidelines for managing HIV infection
Authors: K. M De Cock
Journal: BMJ (1997)

The medical management of HIV infection and AIDS has finally been rewarded with some success, witnessed by falls in AIDS associated deaths in industrialised countries, fewer opportunistic infections, and fewer admissions for HIV infection.1 2 What constitutes optimal practice, however, remains a topic of debate. Two widely publicised sets of guidelines on antiretroviral treatment have appeared over the past year, one from the International AIDS Society in the United States,3 and the other from the British HIV Association.4 While their emphasis was different, the recommendations were broadly similar.

The guidelines agreed on the need for regular monitoring of HIV-1 plasma RNA (“viral load”) and for using antiretroviral treatment in people with low CD4 lymphocyte counts or symptomatic disease. The British guidelines were less prescriptive and placed less emphasis on introducing treatment for people with CD4 cell counts >300x106/l and high viral load.4 Both guidelines endorsed combinations of nucleoside analogues such as zidovudine and didanosine (AZT/ddI), zidovudine and zalcitabine (AZT/ddC), or zidovudine and lamivudine (AZT/3TC) as first line treatments and discussed indications and options for switching treatments.3 4

Practice in many quarters, however, has moved beyond these guidelines.5 6 Many doctors now use triple therapy including a protease inhibitor …
Abstract 4378: Defining the role of mammary stem cells and progenitor cells in the development of estrogen-induced mammary cancer in the rat
Authors: Lina Ding, James D. Shull
Journal: Cancer Research (2011)

Abstract Substantial data implicate both estrogens and progestins in the etiology of breast cancer. However, the mechanisms through which these steroid hormones elicit their effects on breast cancer risk have not been elucidated. The ACI rat serves as a unique model for investigating the mechanisms through which estrogens and progestins contribute to breast cancer development and for defining the genetic bases of inherited risk of breast cancer. When treated with physiologic levels of 17β-estradiol (E2), female ACI rats develop mammary cancer at an incidence that approaches 100%. Interestingly, rapid development of mammary cancer in E2 treated ACI rats is dependent upon progesterone. The mammary cancers that develop in E2 treated ACI rats are estrogen dependent, frequently exhibit non-random patterns of genome instability, and are invasive. Because each of these phenotypes is also commonly exhibited by breast cancers in humans, the ACI rat appears to be highly relevant to the study of breast cancer etiology. Whereas female ACI rats are highly susceptible to E2-induced mammary cancer, female Brown Norway (BN) rats are resistant. Genetic studies performed by our laboratory localized a total of six quantitative trait loci (QTL), designated Emca3 through Emca9, that account for a large fraction of inherited susceptibility in F2 progeny generated in intercrosses between ACI and BN rats. The purpose of this study is to test the hypothesis that ACI and BN rats exhibit differences in the responsiveness of their mammary stem cell (MaSCs) and/or progenitor cell (MaPCs) populations to E2 and/or progesterone. By using a combination of markers CD31, CD45, CD24, CD29 and fluorescence-activated cell sorting, we have identified four distinct populations of mammary cells. To quantify the numbers of MaSC and MaPC in these populations, we are evaluating the ability of the basal (Lin-CD24+CD29high) and luminal (Lin-CD24+CD29low) cell populations to form colonies when cultured in vitro and to generate mamamry gland outgrowths when transplanted into the interscapular fat pad of recipient syngenaic or (ACIxBN)F1 rats. Any observed differeces in MaSC and/or MaPC number or function will be evaluated further using a set of congenic rat strains that harbor BN alleles across an individual Emca locus on the ACI genetic background. 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 4378. doi:10.1158/1538-7445.AM2011-4378
Clinical Findings for Fungal Infections Caused by Methylprednisolone Injections
Authors: Tom M. Chiller, Monika Roy, Duc Nguyen, Alice Guh, Anurag N. Malani, Robert Latham, Sheree Peglow, Tom Kerkering, David Kaufman, Jevon McFadden, Jim Collins, Marion Kainer, Joan Duwve, David Trump, Carina Blackmore, Christina Tan, Angela A. Cleveland, Tara MacCannell, Atis Muehlenbachs, Sherif R. Zaki, Mary E. Brandt, John A. Jernigan
Journal: New England Journal of Medicine (2013)

Since September 18, 2012, public health officials have been investigating a large outbreak of fungal meningitis and other infections in patients who received epidural, paraspinal, or joint injections with contaminated lots of methylprednisolone acetate. Little is known about infections caused by Exserohilum rostratum, the predominant outbreak-associated pathogen. We describe the early clinical course of outbreak-associated infections.We reviewed medical records for outbreak cases reported to the Centers for Disease Control and Prevention before November 19, 2012, from the six states with the most reported cases (Florida, Indiana, Michigan, New Jersey, Tennessee, and Virginia). Polymerase-chain-reaction assays and immunohistochemical testing were performed on clinical isolates and tissue specimens for pathogen identification.Of 328 patients without peripheral-joint infection who were included in this investigation, 265 (81%) had central nervous system (CNS) infection and 63 (19%) had non-CNS infections only. Laboratory evidence of E. rostratum was found in 96 of 268 patients (36%) for whom samples were available. Among patients with CNS infections, strokes were associated with an increased severity of abnormalities in cerebrospinal fluid (P<0.001). Non-CNS infections were more frequent later in the course of the outbreak (median interval from last injection to diagnosis, 39 days for epidural abscess and 21 days for stroke; P<0.001), and such infections developed in patients with and in those without meningitis.The initial clinical findings from this outbreak suggest that fungal infections caused by epidural and paraspinal injection of a contaminated glucocorticoid product can result in a broad spectrum of clinical disease, reflecting possible variations in the pathogenic mechanism and in host and exposure risk factors. (Funded by the Centers for Disease Control and Prevention.).
Abstract 4141: The role of microRNA in gastric cancer
Authors: Jianfang Li, Beiqin Yu, runhua Feng, liping Su, zhenggang Zhu, bingya Liu
Journal: Cancer Research (2012)

Abstract Objectives: To expore miRNA expression pattern in gastric cancer and investigate the role of miRNAs in the tumorigenesis of gastric cancer. Methods: We globally analyzed the miRNA expression profile in 9 gastric cancer cell lines and 6 normal gastric mucosa and the tumor tissues and its corespending adjacent normal tisuues of 30 patients through miRNA microarray. The differential expression of miRNAs from miRNA microarray were confirmed by qRT-PCR. Then, we extended our assay to sixty paired gastric cancer tissues and the relationship between miR-126 expression level and clinicopatholoic variables was explored. The specific miR-126 precursor or miR-126 expression vector were transfected into gastric cancer cell line SGC-7901 to up-regulate miR-126 expression and its biological effects on SGC-7901 cells were investigated. Finally, the target gene of miR-126 was predicted by bioimformatic method and validated by luciferase reportor system. Results: found that 17 miRNAs were up-regulated in gastric cancer cell lines and 146 miRNAs were down-regulated compared with normal gastric mucosa. Then we performed quantitative real-time PCR of 15 up-regulated miRNAs and 26 logRatio &amp;lt; –5.0 down-regulated miRNAs in gastric cancer cell lines and gastric cancer tissues for further analysis. The coincidence of microarray data and qPCR results was in an acceptable range and 15 miRNAs were finally selected. These candidate miRNAs were associated with gastric cancer clinicopathology in different degree. Meanwhile, high expression of hsa-miR-93 and hsa-miR-409-3p were found to predict poor survival (median, 16 months vs 40 months, LogRank p &amp;lt; 0.05). we show that miR-126 is significantly down-regulated in gastric cancer tissues and associated with clinicopathological features such as tumor size, lymph node metastasis, local invasion and TNM stage. Ectopic expression of miR-126 in SGC-7901 gastic cancer cells potently inhibits cell growth by inducing cell cycle arrest at G1 phase, migration and invasion in vitro and tumorigenicity in vivo. Mechanistically, we identify adaptor protein Crk as a target of miR-126. Taken together, our findings demonstrate miR-126 may function as a tumor suppressor in gastric cancer through regulation of genes such as Crk. Conclusions: These findings may suggest vital roles of miRNAs in huamn gastric cancer, and provide clues for understanding the molecular basis of miRNAs in various biological processes. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4141. doi:1538-7445.AM2012-4141
Reduction of Nosocomial Infection during Pediatric Intensive Care by Protective Isolation
Authors: Bruce S. Klein, William H. Perloff, Dennis G. Maki
Journal: New England Journal of Medicine (1989)

To determine whether simple protective isolation reduces the incidence of nosocomial bacterial and fungal infection during pediatric intensive care, we randomly assigned 70 children who were not immunosuppressed and who required mechanical ventilator support and three or more days of intensive care to receive standard care (n = 38) or protective isolation (n = 32) with the use of disposable, nonwoven, polypropylene gowns and nonsterile latex gloves. Risk factors predisposing patients to infection were comparable in the two groups. Nosocomial colonization occurred later among isolated patients (median, 12 vs. 7 days; P<0.01) and was associated with subsequent infection in 2 patients, as compared with 12 patients given standard care (P = 0.01). Among patients who were isolated, the interval before the first infection was significantly longer (median, 20 vs. 8 days; P = 0.04), the daily infection rate was 2.2 times lower (95 percent confidence interval, 1.2 to 4.0; P = 0.007), and there were fewer days with fever (13 percent vs. 21 percent; P = 0.001). The benefit of isolation was most notable after seven days of intensive care. Isolation was well tolerated by patients and their families. Regular monitoring showed that the children in each group were touched and handled comparably often by hospital personnel and family members. We conclude that the use of disposable, high-barrier gowns and gloves for the care of selected, high-risk children who require prolonged intensive care significantly reduces the incidence of nosocomial infection, is well tolerated, and does not compromise the delivery of care. (N Engl J Med 1989; 320:1714–21.)
AB0062 Trem-1 expression induced by vitamin D3 in human monocytes/macrophages
Authors: J.D. Ji, B. Lee, T.-H. Kim, E. Kwon, S.J. Choi, Y.H. Lee, J. Sohn, G.G. Song
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Triggering receptor expressed on myeloid cells-1 (TREM-1) is a recently identified cell surface receptor that is expressed mainly on monocytes and neutrophils, and plays a role as an amplifier of immune response. Recent studies suggested that TREM-1 may play an important role in the pathogenesis of chronic inflammatory diseases such as rheumatoid arthritis (RA) and inflammatory bowel disease (IBD). TREM-1 expression is strongly upregulated by inflammatory stimuli such as lipopolysaccharide (LPS) and prostaglandin E2 (PGE2). <h3>Objectives</h3> In this study, we investigated the regulation of TREM1 expression in human monocyte/macrophages. Also, we examined the effects of vitamin D<sub>3</sub> on TREM-1 expression in human monocyte/macrophages. <h3>Methods</h3> Gene expressions were analyzed using real-time PCR and cell surface expression of TREM-1 was analyzed by flow cytometry. <h3>Results</h3> In human peripheral monocytes, TREM-1 is highly expressed and TREM-1 expression is down-regulated during differentiation into macrophages. In these cells, lipopolysaccharide (LPS) and TNFa, but not IL-1b stimulate TREM-1 expression. In addition to inflammatory molecules such as LPS and TNFa, 1,25-Dihydroxyvitamin D<sub>3</sub> (1,25(OH)<sub>2</sub>D<sub>3</sub>)strongly upregulated the expression of TREM-1 in human monocyte/macrophages. Also TREM-1 expression was upregulated by 1,25(OH)<sub>2</sub>D<sub>3</sub> in synovial fluid macrophages from RA patients. We found that 1,25(OH)<sub>2</sub>D<sub>3</sub> stimulates TREM-1 mRNA expression by augmenting transcription, not by inhibiting mRNA degradation. The upregulated expression of TREM-1 by 1,25(OH)<sub>2</sub>D<sub>3</sub> was partially dependent on p38 MAPK and NF-κB activation, and required new protein synthesis. Finally, 1,25(OH)<sub>2</sub>D<sub>3</sub> augments TREM-1-stimulated IL-1β expression in the presence of LPS suggesting that vitamin D<sub>3</sub>-induced TREM-1 is functional. <h3>Conclusions</h3> Our results show that 1,25(OH)<sub>2</sub>D<sub>3</sub> can affect the innate and inflammatory responses by up-regulating TREM-1 expression, and suggest the possibility that 1,25(OH)<sub>2</sub>D<sub>3</sub> may be function as an enhancer of innate immune response in chronic inflammatory conditions. <h3>Disclosure of Interest</h3> None Declared