tbuckley/cabot-search huggingface dataset:
Gastric perforation into the pericardium
Authors: Ana Grilo, Denise Pinto, Margarida Lopes, José Reina, Paulo Jácome, José Vaz
Journal: Endoscopy (2014)

A 68-year-old man with a previous history of partial gastrectomy (Billroth II) for an unknown indication, was admitted as an emergency case to our hospital following several hours of epigastric pain. He had suffered weight loss and anorexia for about 4 days, without hematemesis or melena. The physical examination findings were normal except for leg edema. Pulse rate was 118 bpm and blood pressure was 101/63 mmHg. Laboratory findings were normal (hemoglobin 11.7 g/dL). Nothing abnormal was observed on chest radiography. Endoscopy revealed a large perforated area at the gastric fundus, with a protruding and strongly pulsatile base, which was mobile and free in relation to the borders ([Fig. 1], [Video 1]). Endoscopic findings suggested gastric perforation into the pericardium, and surgery was decided.
Guidelines for Healthy Weight
Authors: Walter C. Willett, William H. Dietz, Graham A. Colditz
Journal: New England Journal of Medicine (1999)

Excess body fat is a cause of cardiovascular diseases, several important cancers, and numerous other medical conditions1 and is a growing problem in many countries. In the United States, for example, the age-adjusted prevalence of obesity increased by approximately 30 percent from 1980 to 1994.2 In this review we consider the assessment of body fat and the definition of a healthy body weight for an adult. We also discuss how clinicians can use this information in caring for patients. Because overt obesity has undisputed adverse consequences for health, our focus is on lesser degrees of adiposity, the consequences of which . . .
Septic Cerebral Venous Thrombosis
Authors: Slaven Pikija, Johannes S Mutzenbach
Journal: New England Journal of Medicine (2015)

A 71-year-old woman presented after 5 days of right retroauricular pain radiating to the retrobulbar area with accompanying putrid nasal discharge, body chills, double vision, and swelling of the right eye. MRI contrast images showed a partially occlusive thrombus.
Vitamin E Consumption and the Risk of Coronary Disease in Women
Authors: Meir J. Stampfer, Charles H. Hennekens, JoAnn E. Manson, Graham A. Colditz, Bernard Rosner, Walter C. Willett
Journal: New England Journal of Medicine (1993)

Interest in the antioxidant vitamin E as a possible protective nutrient against coronary disease has intensified with the recognition that oxidized low-density lipoprotein may be involved in atherogenesis.
THU0268 Local infliximab injection of sacroiliac joints in early axial spondyloarthropathies: Impact on parameters of disease activity:
Authors: E. Soliman, G. El-tantawy, K. Matrawy, A. Aldawoudy, A. Naguib
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Systemic administration of tumor necrosis factor-alpha (TNF-α) antagonists, such as infliximab, has been shown to be effective in the treatment of spondyloarthropathies (SpA). However, experience with the local use of anti-TNF-α in patients with sacroiliitis, ankylosing spondylitis, or other forms of SpA is limited. The effects of intravenous infliximab therapy on MRI signs of sacroiliac joint (SIJ) activity and on clinical measures of disease activity has been previously demonstrated, however the effects of its local injection into SIJ is not yet studied. <h3>Objectives</h3> To study the effects of local SIJ injection of infliximab on clinical and MRI signs of disease activity in early axial SpA. <h3>Methods</h3> The study included thirty-seven patients fulfilling the ASAS criteria for axial SpA, with disease duration of less than one year, who failed to respond to non-steroidal anti-inflammatory drugs (NSAID). Patients with associated peripheral arthritis, psoriasis or inflammatory bowel disease were excluded. STIR, T2 Fat saturation and T1W MRI of spine and SIJ were performed for all patients. Only those having active sacroiliitis without signs of spondylitis were selected (number = seven patients) to receive fluoroscopic- guided local injection of 20 mg of infliximab in each SIJ. Leeds scoring system was used to score bone marrow edema (BME) representative of active inflammation. MRI of SIJ was repeated six months after the SIJ injection. Patients were clinically evaluated before, three and six months after SIJ injection. This included Bath Ankylosing Spondylitis Disease Activity index (BASDAI), Bath Ankylosing Spondylitis Functional index (BASFI) and Bath Ankylosing Spondylitis Global index (BASGI), back pain and back stiffness scores, in addition to measuring erythrocyte sedimentation rate (ESR). <h3>Results</h3> There was a significant decrease in the mean levels of BASDAI, BASGI, back pain and stiffness scores (table) following local infliximab injection of SIJs. This improvement was detected after three months and was maintained at six months post injection. Furthermore, there was a decrease in the mean BME score, BASFI and ESR but without reaching statistical significance. BME scores decreased in five patients, increased in one patient and remained unchanged in another one, but none of them developed MRI signs of chronic sacroiliitis. <h3>Conclusions</h3> Local infliximab injection of SIJ can be an effective therapeutic option in early axial SpA patients who failed to respond to NSAIDS. This modality can be considered in selected cases to avoid the high cost and side effects of systemically administered anti-TNF-α drugs. Longer period of follow up is needed to detect the maximum duration of disease improvement. <h3>Disclosure of Interest</h3> None Declared
Progressing towards tuberculosis elimination in the European Union and European Economic Area
Authors: M J van der Werf, D Antoine
Journal: Eurosurveillance (2015)

Preview this article: Progressing towards tuberculosis elimination in the European Union and European Economic Area, Page 1 of 1 < Previous page | Next page > /docserver/preview/fulltext/eurosurveillance/20/11/art21066-en-1.gif
The Developing Nature of Menstrual and Reproductive Factors Associated with Breast Cancer Risk among Women in an Urban Region of China.
Authors: J. Gao, B. Zhang, R. Lian, R. Yue, X. Liang, G. Wang
Journal: Cancer Research (2009)

Abstract Introduction: The incidence rate of female breast cancer has increased rapidly over the past 20 years in China. It has become the leading cause of newly diagnosed cancer and a major cause of mortality among women in some large Chinese cities with higher socio-economic status. This was partly explained by the change of lifestyle and reproductive risk factors. However, little data exists on the extent to which the menstrual and reproductive factors with breast cancer risk have changed in other less developed Chinese cities.Method: One cross sectional study was conducted in urban region of Taiyuan of China from September 2008 to March 2009. One thousand and five hundreds healthy women were invited to complete a self-administered questionnaire. Participants' characteristics, including age, education, occupation, weight, height, age at menarche, age at first birth, parity, duration of breastfeeding, and age at menopause were collected and analyzed. Study subjects were divided into six groups: younger than or equal to 20, 21 to 30, 31 to 40, 41 to 50, 51 to 60 and older than 60 years old.Results: One thousand four hundreds and twenty eight women returned the questionnaire. The response rate was 95.2%. Median age of women in this study was 39 years old (range: 16 – 86 years old). There was a 4.8cm difference in the mean height between women born in 1990s and 1940s. The average age at menarche dropped from 16 years for women aged above 60 to 14.3 years for those younger than 20 years old. The average birth rate markedly decreased from 4.4 births per woman in the 1960s to 1.1 births per woman in the 1990s. The mean age at first birth increased 5.6 years through the period from the 1940s to 1980s. The breastfeeding time significantly reduced from 20.3 months to 3.6 months over 40 years.Conclusion: This study indicates that there has been significant change in the menstrual and reproductive factors associated with breast cancer risk in the last 40 years. These changes will certainly influence the incidence rate of breast cancer in the local city. Therefore, measures are needed to enhance the awareness of breast cancer and its early-detection methods among the urban region women in China. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 6068.
MANAGEMENT AND OUTCOMES OF ST-ELEVATION MYOCARDIAL INFARCTION IN RENAL TRANSPLANT RECIPIENTS VERSUS END-STAGE RENAL DISEASE PATIENTS ON DIALYSIS
Authors: Tanush Gupta, Dhaval Kolte, Sahil Khera, Prakash Harikrishnan, Marjan Mujib, Wilbert Aronow, Diwakar Jain, Howard Cooper, William Frishman, Deepak Bhatt, Gregg Fonarow, Julio Panza
Journal: Journal of the American College of Cardiology (2016)
Abstract 5447: Phosphorylation status of Ascl1 regulates neuroblastoma self-renewal and differentiation.
Authors: Luke A. Wylie, Carol J. Thiele, Anna Philpott
Journal: Cancer Research (2013)

Abstract Neuroblastoma (NB) is a tumor of infancy that accounts for 15% of all pediatric cancer mortality. NB bares striking similarity to undifferentiated neuroblasts of the sympathetic nervous system in gene expression profiles and histological appearance. In most neuroblastoma tumors, the cell cycle is hyperactive due to overexpression of cyclin D1 and amplification of MYCN. However, retinoic acid (RA) induces differentiation and cell cycle exit of some NB cell lines in vitro and provides significant benefit to patients in the clinic. As neuroblastoma appears to result from sustained proliferation and inhibition of differentiation, we sought to understand how cell cycle and differentiation are linked within NB. We focused our efforts on Ascl1, a proneural transcription factor that is both necessary and sufficient for neural differentiation of noradrenergic neurons and has been shown to be regulated by the cell cycle. Paradoxically, Ascl1 is both highly expressed and associated with poor prognosis in NB. However, we hypothesized that Ascl1 phosphostatus critically regulates its ability to induce differentiation. We show that Ascl1 is highly expressed and phosphorylated across multiple NB cell lines and is largely phosphorylated by CDKs. Phosphorylated Ascl1 actively promotes the G1-S transition by upregulating E2f, Skp2, and Cdk2. These targets all promote CDK activity, further maintaining Ascl1 phosphorylation. However, a phosphomutant form of Ascl1, where putative CDK sites are mutated, arrests cells in the G1 phase by preferentially upregulating Ebf3 and p27. These targets inhibit CDK activity promoting Ascl1 dephosphorylation and further upregulation of Ebf3 and p27. We propose a model whereby Ascl1 sits between two positive feedback loops, both forming a critical link between cell cycle and differentiation, but also as an agent to commit cells to either a self-renewing undifferentiated state or a postmitotic differentiated state. Given this model, we hypothesized that pharmacologic inhibition of CDK activity when combined with a pro-differentiation agent such as RA would synergistically cause differentiation in neuroblastoma. Indeed, CDK inhibitor and RA combination treatment causes increased differentiation in RA-susceptible cell lines and induces differentiation in RA-resistant cell lines. Given that most neuroblastoma tumors have an overactive cell cycle and also highly express Ascl1, combination therapy of CDK inhibitor and RA may provide generalized benefit to NB patients. Citation Format: Luke A. Wylie, Carol J. Thiele, Anna Philpott. Phosphorylation status of Ascl1 regulates neuroblastoma self-renewal and differentiation. [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 5447. doi:10.1158/1538-7445.AM2013-5447
Endosonographic and Clinicopathological Features of polypoid lesions at Gastroesophageal Junction Associated with Reflux Esophagitis
Authors: CJ Lin, CT Chiu, YY Chu, JM Lien, PC Chen
Journal: Endoscopy (2006)

Background and Aims: Gastric polyps at gastroesophageal junction (GEJ) are found incidentally when EGD is performed for GERD. The pathologic nature and malignant potential of superficial protruding lesions are difficult to be confirmed by either EUS or EGD biopsy. The study was to evaluate the EUS features and clinicopathologic outcomes of GEJ polypoid lesions. Patients and methods: From Jul 1999 to Dec 2005, total 65 patients with reflux esophagitis and polypoid lesions (>5mm) at GEJ are referred for EUS. EUS pictures/video review was conducted of GEJ superficial polypoid lesions, excluding submucosal tumors. All 48 GEJ polypoid lesions were scanned by Olympus UM-2R/3R miniprobes and water-filling method, followed by 17 endoscopic resections (4 polypectomy and 13 EMRC) on 16 patients and 32 biopsies for histologic confirmation Results: 48 pts (32 male, 16 female) had mean age 51.2 years (range 19–89 years), and average size by EUS measurement, 9.02+/-4.5mm (4 to 25mm). The final pathology of GEJ polyps: 42 non-neoplastic (25 inflammatory, 17 hyperplastic), 6 neoplastic polyps (3 adenoma and 3 adenocarcinoma. The EUS features of non-neoplastic polyps are ill-defined margin (36/42), hypoechoic mucosal thickening/folding (38/42), central hyperechoic submucosal core (25/42); However that of neoplastic lesions: well-defined margin (5/6), irregular mucosal surface with ulcer/depression (4/6), deep infiltration on muscular layer (1/6). All three adenocarcinoma and one adenoma with severe dysplasia received EMRC, size/age: 13.2mm/84, 12mm/89, 10mm/77, 16.8mm/76 respectively. There is no malignant change on other GEJ polyps from endoscopic follow-up in 2.9yrs. Conclusions: inflammatory and hyperplastic polyps at GEJ are frequently found and predicted by EUS on GERD. Advanced Endoscopic resection methods (eg. EMR) could be applied safely on patient (>70 yr), polyp size (>10mm) and neoplastic polyps.
155 EFFICACY AND SAFETY OF STANDARD ANTIVIRAL THERAPY IN CIRRHOTIC PATIENTS AWAITING LIVER TRANSPLANTATION (LT)
Authors: M.-C. Londoño, G. Crespo, J.-A. Carrión, M. García-Retortillo, Z. Mariño, S. Lens, C. Fondevila, J.-C. García-Valdecasas, M. Navasa, X. Forns
Journal: Journal of Hepatology (2013)
Induction of cell cycle arrest and apoptosis in breast cancer cells by troglitazone, a peroxisome proliferator-activated receptor-gamma (PPAR-γ) ligand.
Authors: H Youn, B Lee, S Jung, M Park, J Yoon, J Lee, M Choi
Journal: Cancer Research (2009)

Abstract Abstract #5034 Background: Peroxisome proliferator-activated receptor-gamma(PPAR-γ) ligands inhibit cell proliferation and induce apoptosis in cancer cells. And, it is reported that PPAR-γ ligands could serve as negative regulators of breast cancer development and progression, but their mechanism is still unknown. Here we wished to determine whether the PPAR-γ ligand induces cell cycle arrest and apoptosis of MDA-MB-231(ERα-negative) and MCF-7(ERα-positive) breast cancer cell.&amp;#x2028; Methods: The effect of PPAR-γ ligands on the cell viability of breast cancer cells was determined using mitochondrial tetrazolium(MTT) assay. The cell cycle distribution and apoptosis induction were evaluated by using the flow cytometry. The expression of apoptosis-related proteins were measured with Western blot analysis. Statistical analysis was performed using Student's t test, and p&amp;lt;0.05 was considered significant.&amp;#x2028; Results: The treatment of MDA-MB-231 cell with PPAR-γ ligand, troglitazone was shown to induce cell cycle G1 arrest and induction of apoptosis. Moreover, troglitazone treatment, applied in a dose-dependent manner, caused a marked decrease in phosphorylated retinoblastoma(pRb), cyclin D1, D2, D3, cyclin dependent kinase(Cdk) 2, 4, and 6 expression as well as a significant increase in Cdk inhibitor, p21 and p27. Troglitazone showed antiproliferative effect on MCF-7 cell with tamoxifen, respectively and synergically. Troglitazone and tamoxifen could induce G1 arrest and apoptosis of MCF-7 cell, through upregulation of Bax and downregulation of Bcl-2 and cyclin D1.&amp;#x2028; Conclusion: PPAR-γ ligand, troglitazone induces cell cycle arrest and apoptosis of MDA-MB-231 cell and increases the sensitivity of anti-hormonal therapy in MCF-7 cell. These results suggest that troglitazone has anticancer effect on both ERα-negative and positive breast cancer cells. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 5034.
Carfilzomib Triggers Cell Death in Chronic Lymphocytic Leukemia by Inducing Proapoptotic and Endoplasmic Reticulum Stress Responses
Authors: Betty Lamothe, William G. Wierda, Michael J. Keating, Varsha Gandhi
Journal: Clinical Cancer Research (2016)

Abstract Purpose: Carfilzomib, while active in B-cell neoplasms, displayed heterogeneous response in chronic lymphocytic leukemia (CLL) samples from patients and showed interpatient variability to carfilzomib-induced cell death. To understand this variability and predict patients who would respond to carfilzomib, we investigated the mechanism by which carfilzomib induces CLL cell death. Experimental Design: Using CLL patient samples and cell lines, complementary knockdown and knockout cells, and carfilzomib-resistant cell lines, we evaluated changes in intracellular networks to identify molecules responsible for carfilzomib's cytotoxic activity. Lysates from carfilzomib-treated cells were immunoblotted for molecules involved in ubiquitin, apoptotic, and endoplasmic reticulum (ER) stress response pathways and results correlated with carfilzomib cytotoxic activity. Coimmunoprecipitation and pull-down assays were performed to identify complex interactions among MCL-1, Noxa, and Bak. Results: Carfilzomib triggered ER stress and activation of both the intrinsic and extrinsic apoptotic pathways through alteration of the ubiquitin proteasome pathway. Consequently, the transcription factor CCAAT/enhancer-binding protein homology protein (CHOP) accumulated in response to carfilzomib, and CHOP depletion conferred protection against cytotoxicity. Carfilzomib also induced accumulation of MCL-1 and Noxa, whereby MCL-1 preferentially formed a complex with Noxa and consequently relieved MCL-1′s protective effect on sequestering Bak. Accordingly, depletion of Noxa or both Bak and Bax conferred protection against carfilzomib-induced cell death. Conclusions: Collectively, carfilzomib induced ER stress culminating in activation of intrinsic and extrinsic caspase pathways, and we identified the CHOP protein level as a biomarker that could predict sensitivity to carfilzomib in CLL. Clin Cancer Res; 22(18); 4712–26. ©2016 AACR.
Abstract 1078: Rosiglitazone inhibits breast cancer growth and proliferation via cyclin D1 inhibition.
Authors: Elaine Oberlick, LaTonia D. Taliaferro-Smith, Wayne Harris, Brandi B. Knight, Arumugam Nagalingam, Edmund Waller, Dipali Sharma
Journal: Cancer Research (2010)

Abstract Breast cancer ranks as the most commonly diagnosed and second leading cause of cancer death in North American women. Thiazolidinediones (TZDs) are a class of anti-diabetic drugs primarily used to treat type 2 diabetes mellitus by increasing insulin sensitivity; these compounds are also known to possess anti-tumor effects in several cancer cells including lung and breast cancer. The present study was designed to evaluate the antiproliferative effects of Rosiglitazone on triple negative breast cancer cells. MDA-MB-231 breast cancer cells were treated with Rosiglitazone and compared with negative control (without treatment) for modulation of molecules involved in cell-cycle regulation and apoptosis, including cyclin D1, caspase-3 and −9, Bad, and Bax. Our results show that Rosigliatzone suppresses the proliferation of highly-metastatic human breast cancer MDA-MB-231 cell line by increasing the number of cells in G1 and reducing the number of cells progressing through the S-phase of the cell cycle. Further investigation revealed that the mechanism by which Rosiglitazone arrested cells in the G1-phase was via inhibition of cyclin D1 (a cell cycle regulatory protein that is essential for progression through the G1-phase of the cell cycle and has an central pathogenetic role in breast cancer). Our lab has previously shown an essential role of cyclin D1 upregulation in breast cacner growth and proliferation. Collectively, our results suggest that Rosiglitazone inhibits cancer cell proliferation by modulating expression of cyclin D1 and may provide a novel role for the use of Rosiglitazone as a therapeutic antitumorigenic agent. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1078.
A1.2 Fibroblasts Influence Lymphocyte Recruitment and Migration During Resolving and Persistent Arthritis
Authors: Helen M McGettrick, Andrew Filer, Karim Raza, Gerard B Nash, Christopher D Buckley
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background and Objectives</h3> Fibroblasts actively regulate the recruitment of leukocytes by endothelial cells (EC), acting in a pro- or anti-inflammatory manner depending on their site of origin. The phenotype of the fibroblast may be a critical determinant of whether leukocyte recruitment, and therefore inflammation, resolves or persists. Here we examined how synovial fibroblasts from different stages of arthritis influenced the recruitment of peripheral blood lymphocytes (PBL) and their onward migration. <h3>Materials and Methods</h3> Fibroblasts were isolated from patients with resolving or persistent arthritis. Rheumatoid arthritis (RA) cohorts were categorised based on the stage of the disease at the time of sample collection: very early; newly presented but established or long established undergoing replacement surgery. Two forms of co-cultures were developed: (1) To assess effects on recruitment, EC and fibroblasts were cultured on opposite sides of porous philtres and incorporated into a novel flow chamber. PBL were perfused and observed as they bind to the EC surface. (2) To examine effects on migration, EC monolayers were formed on a philtre above a collagen gel in which fibroblasts were incorporated. PBL migration through the construct and their location within the gel were assessed. Conditioned media from co-cultures were collected and analysed by Luminex. <h3>Results</h3> Fibroblasts from patients with RA increased the ability of EC to support PBL recruitment from flow in a disease duration-specific manner, with binding increasing from very early &lt; established &lt; replacement. However, levels of binding to very early RA co-cultures were similar to those observed when fibroblasts from non-inflamed or resolving tissue were incorporated. In the multi-cellular gel model, all fibroblasts, expected those from non-inflamed tissue, promoted PBL transendothelial migration but had no effect on entry into the gel construct. Interesting, a greater proportion of PBL migrated into the lower half of the gel when fibroblasts from patients with very early and established RA were incorporated. Elevated levels of IL-6, IL-1β, IL-8, Groα and IP-10 were detected in the supernatants from RA co-cultures compared to resolving co-cultures. Resolving fibroblasts dramatically reduced the secretion of these soluble mediators by EC, suggesting they potentially have a suppressive effect. <h3>Conclusions</h3> Collectively these initial data indicate that changes in the ability of fibroblasts to influence endothelial and lymphocyte behaviours may occur very early in the development of RA. Moreover, some of these changes are distinct from the phenotype exhibited by fibroblasts taken from non-inflamed tissue and acutely resolving arthritis.
Minimal amounts of kindlin-3 suffice for basal platelet and leukocyte functions in mice
Authors: Sarah Klapproth, Federico A. Moretti, Marlis Zeiler, Raphael Ruppert, Ute Breithaupt, Susanna Mueller, Rainer Haas, Matthias Mann, Markus Sperandio, Reinhard Fässler, Markus Moser
Journal: Blood (2015)