tbuckley/cabot-search huggingface dataset:
THE ASSOCIATION OF LIVING IN FOOD DESERTS WITH CARDIOVASCULAR RISK FACTORS AND SUBCLINICAL VASCULAR DISEASE
Authors: Heval Mohamed Kelli, Hina Ahmed, Muhammad Hammadah, Matthew Topel, Salim Hayek, Mosaab Awad, Keyur Patel, Brandon Gray, Kareem Mohammed, Yi-An Ko, Laurence Sperling, Tene T. Lewis, Greg Martin, Gary Gibbons, Arshed Quyyumi
Journal: Journal of the American College of Cardiology (2016)
PARE0008 “Move to improve” – physical activities among inhibitants of WARSAW
Authors: J. Grygielska
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Physical activity is one of conditions for healthy life. According theme of World Arthritis Day 2011-2012 Association of People with Rheumatism and their Friends together with Institute of Rheumatology in Warsaw decided to check level of physical activities and opinion of them among inhibitandts of Warsaw. There is not tradition of physical activities in Poland. It’s one of reason that many people living with long-term conditions like rheumatic diseases are active only during medical rehabilitation. <h3>Objectives</h3> Main objective was to know opinions and interesting in physical activities of people. It was interesting if bad tradition is changing or not and what kinds of activities are more popular than others. <h3>Methods</h3> There was questionnaire prepared in Department of Epidemiology and Health Promotion of Institute of Rheumatology. This questionnaire was given to complete to visitors of stand of Association of People with Rheumatism and their Friends. Stand was available during healthy event in Warsaw: district picnic, central picnic in Warsaw on occasion of International Day of Older People and during WAD event in Institute of Rheumatology. During 3 days 160 questionnaires were completed. People were asked: how often they are active, causes of inactivity, choice of preffered activity, their own experiences of living with rheumatic diseases and benefits of activity for people with rheumatic diseases. <h3>Results</h3> Women were majority of respondents (83%). 51% of respondents were in age over 60 years. Great majority of them (91%) are physically active - 52% more than once a week, 41% - 2-3 times monthly. People inactive gave as main cause of it (44%) - lack of desire. From proposed activities rhe most popular was cycling and swimming (both at 28%). Almost all declared that physical activities are good for people living with rheumatic diseases - 54% of respondents are living with those diseases themselves. <h3>Conclusions</h3> Inhibitants of Warsaw participated in healthy events know benefits of phycical activities. There are physically active in the majority of not less than 2-3 times monthly. It’s a good prognostic for future - physical activity is an element of healthy ageing. <h3>Disclosure of Interest</h3> None Declared
Isolated gastroduodenal Crohn’s disease in a septuagenarian man
Authors: Jatinder Goyal, Ali Khan, Anshum Goel, Frederick Weber
Journal: Endoscopy (2014)

Isolated gastroduodenal Crohn's disease (GCD) is extremely rare. We hereby report a unique case of isolated GCD masquerading as apparent linitis plastica in an elderly man. A 78-year-old Caucasian man with an insignificant past medical history was referred to our gastroenterology service with intractable nausea and vomiting of gradually increasing frequency over 2 years. [Table 1] summarizes the results of his laboratory tests.
Abstract 117: The processed pseudogene <i>POU5F1P1</i>in 8q24 is expressed in tumor and shows oncogenicity
Authors: Jun Fang
Journal: Cancer Research (2012)

Abstract Genome-wide association studies (GWAS) have identified a segment of approximately 1 Mb of 8q24 as a multi-cancer cancer susceptibility region. The region is flanked by two genes, FAM84B and MYC, the latter an established oncogene. Within this region of 8q24, there is a processed pseudogene, POU5F1P1. We have re-sequenced the exon regions of wild type POU5F1 on chromosome 6 and its six counterpart pseudogenes on chromosomes 1, 3, 8, 10 and 12, and identified sequence variants unique to POU5F1P1 for which we have developed and confirmed analysis of expression of the POU5F1P1 transcript on 8q24. The homolog between wild type POU5F1 and pseudogene POU5F1P1 is about 97%. By using TaqMan DNA copy number variation assays, we identified uncommon copy number variants across this region. However, the DNA copy number variation does not contribute to differences in expression of POU5F1P1. Expression of POU5F1P1 was confirmed in a subset of the NCI60 panel using quantitative TaqMan real-time PCR assays in cell lines of colon, ovarian and breast cancers. Both POU5F1 and POU5F1P1were further evaluated in 14 colon cancer cell lines of which two, DLD-1 and KM12, expressed POU5F1P1 but no wild type POU5F1. Using shRNA technology (two constructs for each target), we knocked down POU5F1P1 expression in DLD-1 and KM12, which lead to reduction in the growth rate and anchorage-independent growth of colon cancer cells. Our results suggest that the processed pseudogene, POU5F1P1 is expressed in cell lines and colon cancer tissues. Moreover, preliminary studies suggest that its function could be related to oncogenic activity, though further studies are needed to verify this observation. 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 117. doi:1538-7445.AM2012-117
AB0388 Coexistence of systemic lupus erythematosus and multiple sclerosis. prevalence and natural history
Authors: A. Fanouriakis, V. Mastorodemos, C. Pamfil, P. Sidiropoulos, G. Bertsias, D. T. Boumpas
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Although segregation of systemic lupus erythematosus (SLE) and multiple sclerosis (MS) has been reported within families with multiple members affected with autoimmune diseases, coexistence of the two disorders in the same individual has only rarely been described. <h3>Objectives</h3> To describe the clinical characteristics of patients fulfilling the criteria for both SLE and MS. <h3>Methods</h3> We reviewed the medical records, laboratory and neuroimaging findings in six patients diagnosed with both SLE (ACR 1987 criteria) and MS (2010 revised McDonald criteria). Cases were identified from existing cohorts of patients with SLE (<i>n</i> = 728) and MS (<i>n</i> = 819), followed in the Departments of Rheumatology and Neurology, University of Crete. <h3>Results</h3> All six patients were women, with an average age of SLE diagnosis at 44 years (Table), which is relatively higher from the usual age of disease onset. Antiphospholipid antibodies (aPLs) were present in two patients (33%), but none fulfilled criteria for antiphospholipid syndrome. In five patients, the diagnosis of SLE preceded the development of MS, in four of them with a time lag of ≤ 5 years (median 4 years, range from 2 to 16 years). Only one patient (case #2) had a long-standing (&gt;20 years) history of relapsing-remitting MS (RRMS) before developing SLE. Clinical presentation of MS included spinal symptoms in five patients. All patients had mild SLE with cutaneous, mucosal and musculoskeletal manifestations, and only case #3 had history of pericarditis. Accordingly, therapeutic decisions were mainly guided by the severity of the neurological syndrome (Table). During median follow-up of 4 years (range 1-9 years), three patients remained stable and the remaining experienced gradual deterioration in their neurological status. SLE remained quiescent in all patients with standard immunomodulatory MS therapy. <h3>Conclusions</h3> Although SLE and MS may have overlapping features, occurrence of patients fulfilling criteria for both diseases is rare, confirming microarray findings for distinct molecular signatures[1]. In our cohort, SLE and MS co-existence was not associated with a severe phenotype for both entities. Longitudinal, larger cohorts in other ethnic groups are needed to further verify these findings. <h3>References</h3> Feng X, Reder NP, Yanamandala M, Hill A, Franek BS, Niewold TB, et al. Type I interferon signature is high in lupus and neuromyelitis optica but low in multiple sclerosis. J Neurol Sci. 2012 Feb 15; 313(1-2):48-53. <h3>Disclosure of Interest</h3> None Declared
Case 2-2012
Authors: Darrell N. Kotton, Victorine V. Muse, Michiya Nishino
Journal: New England Journal of Medicine (2012)

A 63-year-old woman was admitted to the hospital because of respiratory failure. She had a history of granulomatous polyangiitis and a breast implant that had recently become painful. Imaging revealed bilateral pulmonary infiltrates and a soft-tissue mass extending from the implant through the chest wall.
Metastatic Melanoma to the Thyroid Gland Expressing Somatostatin Receptors—Imaging With 68Ga-DOTANOC PET/CT
Authors: Rayamajhi Sampanna Jung, Bhagwant Rai Mittal, Amanjit Bal, Pranab Dey, Jaya Shukla, Rakesh Kapoor
Journal: Clinical Nuclear Medicine (2014)

Malignant melanoma is an aggressive tumor with poor prognosis that can have widespread metastases at presentation. Melanoma is known to undergo neuroendocrine differentiation. We report a case of a 60-year-old woman with malignant melanoma showing a metastatic lesion in the thyroid expressing somatostatin receptors as evident by Ga-DOTANOC PET/CT and metabolically active widespread subcutaneous metastases on F-FDG PET/CT imaging.
Dynamic magnet resonance tomography for monitoring the efficacy of an anti-vascular tumor therapy by paclitaxel encapsulating cationic lipid complexes (MBT-0206)
Authors: M. E. Eichhorn, S. Becker, S. Strieth, A. Werner, B. Sauer, H. Ruhstorfer, U. Michaelis, J. Griebel, G. Brix, K. W. Jauch, M. Dellian
Journal: Cancer Research (2004)

1310   Systemically administrated cationic lipid complexes accumulate selectively in angiogenic tumor endothelium1,2. The chemotherapeutic agent paclitaxel was encapsulated into these lipid complexes, providing an anti-neovascular targeting agent (MBT-0206) with strongly enhanced anti-tumor activity3,4. In the current study the effect of MBT-0206 on the tumor vasculature was measured by dynamic magnet resonance tomography (dMRT). On day 5, 6 and 7 after subcutaneous inoculation of A-MEL 3 tumor cells into Syrian golden hamsters, the animals were treated by i.v. injection of MBT-0206 or Taxol, both at a dose of 5 mg paclitaxel/kg, followed by dMRT measurements at day 8. Untreated tumors were analyzed as a control. Before and after intravenous injection of the contrast agent Gd-DTPA, dynamic T1-measurements were performed with Snapshot FLASH-sequences using a high resolution MRT (9,4 Tesla) in the tumor and the arterial blood over 60 min. From the contrast-time curves the regional blood volume (BV) and the permeability-surface product within the tumor were calculated, followed by harvesting the tumors for histological analysis. The treatment with MBT-0206 resulted in a significant inhibition of tumor growth compared to the Taxol and the control group. The intra-tumoral BV of MBT-0206 treated animals was significantly reduced by 34% compared to the control group. In addition, the vascular permeability in the MBT-0206 treated tumors was increased, resulting in a 2-fold slower clearance of Gd-DTPA within the tumor. In contrast to MBT-0206, Taxol treatment revealed no MRI effects. Immunohistochemical analysis revealed a significant reduction of the microvascular density in the MBT-0206 treated tumors by 50%. The anti-vascular tumor therapy with paclitaxel encapsulated in cationic lipid complexes (MBT-0206) resulted in a potent functional impairment of the tumor microcirculation. Dynamic magnet resonance tomography as a non-invasive technique represents an useful approach to quantify these anti-vascular treatment effects. Thereby it provides an attractive surrogate measure of the therapeutic effectiveness and mode of action of MBT-0206 in clinical trials. 1Thurston et al., J Clin Invest 101: 1401-13, 1998 2Krasnici et al., Int J Cancer 105: 561-7, 2003 3Schmitt-Sody et al., Clin Cancer Res 9: 2335-41, 2003 4Kunstfeld et al., J Invest Dermat 120: 476-82, 2003
DECIPHERING INTRINSIC AND ADAPTIVE RESISTANCE TO PI3K PATHWAY INHIBITORS IN GLIOMA
Authors: W. K. A. Yung, D. Koul, S. Wu, J. Fu
Journal: Neuro-Oncology (2014)

BACKGROUND: Glioblastoma represents a compelling disease for signal transduction targeted therapy. Despite the evidence defining the PI3K network as a high quality target, regulatory feedback loops as well as cross talk with other networks make targeting the PI3K network a challenging task. Complete control of GBM is dependent on the elucidation of the escape mechanisms and the rational design of combination therapies. A major objective in our laboratory is to develop robust predictive molecular and genetic markers/signature that will lead to selection precision therapy. These predictive markers will allow us to determine rational combinatorial approaches to target aberrations in the PI3K network and at the same time prevent deleterious effects of feedback loops and cross talk. METHODS: We have utilized a large panel of glioma stem cell (GSC) lines to perform drug sensitivity/resistance screens. Reponses profiles of GSCs using multiple PI3K inhibitors in cytotoxicity assay were generated. Molecular targets/pathways contributing to alternate signaling pathway activation by inhibitors were identified using gene expression profiling and protein expression/activity profiling. Top gene targets were subjected to loss of function studies using RNAi. Synergistic effect of knocking down the target along with PI3K inhibitors on cell proliferation, and tumorigenicity were assessed. RESULTS: We have utilized several system approaches to identify targets in compensatory or parallel pathways after PI3K inhibition. Our results suggest that different molecular profiles in GSC dictate the differences in viability observed after drug treatment, despite a common blockade of PI3K pathway. Resistant and sensitive cell lines were profiled using the Affymetrix and RPPA platforms to identify genes that are differentially expressed in sensitive and resistant GSCs responsible for intrinsic resistance. Using gene expression profiling, we also identified adaptive response gene targets in pre- and post-treatment resistant GSC. This approach has uncovered alternate pathways and shutting down these pathways would synergize the effect on cell growth when combined with PI3K pathway inhibitors. We have selected the top 10 candidate genes and two targets are being studied for rational combination with PI3K inhibitors CONCLUSIONS: Failure of PI3K pathway inhibitors is due to escape through overlapping or parallel signaling pathways, and that complete control of GBM depend on the elucidation of these escape mechanisms and we show that therapies to target essential pathways overcome or circumvent treatment resistance and can provide the next generation of improved therapeutic options. SECONDARY CATEGORY: Tumor Biology.
Do trusts ensure their workers are immune to measles, mumps, and rubella?
Authors: R. Mearkle, H. Cheney, M. Mindlin
Journal: BMJ (2013)

Background/Aim: The mutational status of stage III and IV melanomas should be recognized in order to allow for targeted therapies. The aim of our study was the characterization of BRAF, NRAS and C-KIT melanoma patients, in order to define their optimal management. Patients and Methods: Between 1991 and 2015, 63 mutated melanoma patients were treated and monitored during their diagnostic and therapeutic management at a single institution. Results: BRAF-mutated melanoma patients were the most common, representing 70% of the study population, while NRAS- and C-KIT-mutated melanoma represented 19% and 11% respectively. BRAF-mutated melanomas were mostly located at sites of intermittent sun exposure, and were associated with higher Breslow thickness and an increased number of mitosis. NRAS mutated melanoma were mainly observed in chronic sun-damaged areas and had a negative prognostic value, with shorter time to progression and a high incidence of central nervous system involvement. C-KIT mutated melanoma were located at acral and mucosal sites. Overall survival observed in the three groups of patients revealed wide differences. Conclusion: BRAF, NRAS and C-KIT melanomas constitute distinct clinico-pathological entities. BRAF-mutated melanoma benefit from both anti-BRAF and anti-MEK targeted therapies while triple-negative melanomas could benefit from novel anti-CTLA-4 and anti-PD-L1 immunotherapeutic approaches.
Case 38-1999
Authors: Jeffrey M. Slaiby, Chieh-Min Fan, H. Thomas Aretz
Journal: New England Journal of Medicine (1999)

Presentation of CaseA 62-year-old woman was admitted to the hospital because of a foot infection.The patient's medical history included hypertension, hyperlipoproteinemia, and mild chronic renal failure, with a base-line creatinine level of 2 mg per deciliter (177 μmol per liter). Twelve years before admission, Takayasu's arteritis, severe aortic atherosclerosis, and peripheral vascular disease (central aortic systolic pressure, 130 mm Hg; systolic pressure in each arm, 80 mm Hg) were diagnosed, and prednisone was administered for two years. At approximately the same time, pulmonary hypertension was documented by a catheter study. During the year before the current admission, bilateral . . .
A8.6 Interleukin 33 skin overexpression does not induce inflammation
Authors: Olga Wagner, Verena Kästele, Verena Schmitt, Anja Derer, Dieter Engelkamp, Derek Gilchrist, Iain B McInnes, Georg Schett, Silke Frey, Axel J Hueber
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> The cytokine interleukin 33 (IL-33), a member of the IL-1 family, is released in response to various types of endothelial or epithelial cell damage. IL-33 is constitutively expressed in epidermal keratinocytes, upregulated in inflamed skin and acts as an endogenous danger signal that mediates the recruitment of immune cells to sites of cellular damage. Our preliminary data have shown that psoriatic lesions express more nuclear IL-33 compared to perilesional biopsies from the same patients and mature IL-33 induces skin inflammation in a mouse model. <h3>Objectives</h3> To determine the role and function of IL-33 in skin inflammation, in particular to understand the mechanism how IL-33 contributes to the pathology and recruitment of inflammatory cells. <h3>Materials and Methods</h3> Transgenic mice with skin-specific expression of full length IL-33 were generated via pronuclear injection of K14-IL-33. This construct with IL-33 under keratin 14 promotor was tested for the functionality in vitro following the generation of the transgenic mice. For analysis control littermates with no transgene were used. K14-IL-33 mice were tested in various skin inflammation models including TLR7 agonistic stimulation with imiquimod 5%, ear injection model (rIL-23, 500 ng/ear for 14 days), and skin tape stripping. As readout we used caliper measurement of the ear thickness, skin histology H&amp;E staining and immunohistochemistry as well as mRNA expression by quantitative RT-PCR. <h3>Results</h3> Pronuclear injection resulted in 16 pups with 2 transgenic mice expressing the IL-33 transgene. K14-IL-33 mice were born and developed normally with no obvious phenotype. Increased expression in the skin in K14-IL-33 compare to wildtype (WT) mice was detected using RT-PCR and immunohistology; as expected IL-33 was localised in the nuclei of the keratinocytes. No significant expression was measured in other organs. Due to the lack of a skin phenotype we performed different skin inflammation models in the K14-IL-33 mouse. Neither TLR7 stimulation via imiquimod, ear injection of IL-23, a pivotal cytokine for psoriasis, nor skin tape stripping as a model for chronic skin damage induced a clinical/histological change compared to littermates. <h3>Conclusions</h3> We demonstrate that local skin overexpression of the alarmin IL-33 does not induce spontaneous or triggered skin inflammation. In comparison to a published K14-IL-33 mouse with atopic inflammatory phenotype our data could not reproduce the described phenotype. These data suggest that different expression thresholds might lead to exacerbation of skin diseases.
Emerging Uses for Genomic Information in Drug Discovery
Authors: S H Friend, A Oliff
Journal: New England Journal of Medicine (1998)

Geneticists who study yeast, worms, and fruit flies have long recognized that an effective way to identify genes with functional relevance to a particular biologic process is to screen large numbers of mutagenized organisms. Researchers have recently used these primitive organisms to pinpoint genetic mechanisms in human diseases. This approach has succeeded mainly because genome-sequencing projects have discovered numerous invertebrate homologues of human genes. The gene involved in basal-cell carcinoma, for example, was cloned in part through its similarity to the patched gene of the fruit fly Drosophila melanogaster. 1,2 New work on two breast-cancer–susceptibility genes, BRCA1 and BRCA2, is . . .
Two Meningiomas Detected Incidentally by Tc-99m HDP Bone Scintigraphy During a Work-Up for Breast Cancer
Authors: G K Lee, M Coel, J Ko, B Tom
Journal: Clinical Nuclear Medicine (1999)

A 64-year-old woman was diagnosed with infiltrating ductal carcinoma of the left breast by needle biopsy. Results of a Tc-99m HDP bone scan were normal, except for two areas of increased uptake in the head - one in the left posterior frontal bone and the other in the left sphenoid wing. These findings were investigated further. A plain film study showed a blastic abnormality in the left posterior frontal area. An MRI confirmed two contrast-enhancing lesions adjacent to bone, corresponding to the abnormalities on the bone scans. The findings are consistent with benign meningiomas. The patient subsequently underwent a left modified radical mastectomy. If the lesions on bone scan had not been further evaluated, the patient's cancer would have been categorized stage IV instead of stage I (T1NOMO), which carries a much better prognosis. The patient continues to remain free of neurologic symptoms, so surgery is not being considered at this time.
Tuberculosis in New York City — Turning the Tide
Authors: Thomas R. Frieden, Paula I. Fujiwara, Rita M. Washko, Margaret A. Hamburg
Journal: New England Journal of Medicine (1995)

From 1978 through 1992, the number of patients with tuberculosis in New York City nearly tripled, and the proportion of such patients who had drug-resistant isolates of Mycobacterium tuberculosis more than doubled.