tbuckley/cabot-search huggingface dataset:
IMPACT OF A DISPOSABLE STERILE RADIATION SHIELD ON OPERATOR RADIATION EXPOSURE DURING PERCUTANEOUS CORONARY INTERVENTION OF CHRONIC TOTAL OCCLUSIONS
Authors: Deborah Shorrock, Georgios Christopoulos, Jedrek Wosik, Anna Kotsia, Bavana Rangan, Shuaib Abdullah, Daisha Cipher, Subhash Banerjee, Emmanouil Brilakis
Journal: Journal of the American College of Cardiology (2015)
Is<i>Haemophilus influenzae</i>Meningitis Contagious?
Authors: Arnold L. Smith
Journal: New England Journal of Medicine (1979)

At least two generations of grandmothers are responsible for the hysteria that usually surrounds a case of fulminant meningitis. Epidemics of "cerebrospinal, spotted fevers" in the United States in the 1880's, 1917–1918 and 1942–1943 gave rise to an almost instinctive fear of meningitis. Each case of the dreaded disease (meningococcal sepsis or meningitis) brought concern that it might be the harbinger of a new epidemic. Grandmother was correct about the contagiousness of meningococcal disease; the secondary attack rate exceeds the primary rate in the general population by 700-fold1 — a risk that prompts prophylactic intervention.On the other hand, an . . .
THU0041 Autoreactive Long-Lived Plasma Cells in Nzb/W Mice and their Regeneration
Authors: A. Taddeo, L. Khodadadi, Q. Cheng, A. Radbruch, F. Hiepe, B.F. Hoyer
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Autoantibodies contribute significantly to the pathogenesis of systemic lupus erythematosus (SLE). The long-lived plasma cells (LLPC) secreting such autoantibodies are refractory to conventional immunosuppressive treatments. Although they are generated long before the disease becomes clinically apparent, it is unknown whether their generation continues in the established disease. <h3>Objectives</h3> Here, we analyze the generation of autoreactive LLPCs in lupus-prone NZB/W F1 mice over their lifetime, and LLPC regeneration after depletion. <h3>Methods</h3> BrdU pulse-chase experiments were used to follow the establishment of the LLPS compartment. Bortezomib and cyclophosphamide therapy was used to deplete the LLPCs. <h3>Results</h3> Autoreactive LLPCs are established in the spleen and bone marrow of lupus-prone mice very early in ontogeny, before week 8 and before the onset of symptoms. The generation of LLPCs then continues throughout life. LLPC counts in the spleen plateaued by week 10, but continued to increase in the bone marrow. When LLPCs are depleted by the proteasome inhibitor bortezomib, their numbers regenerate within two weeks. Persistent depletion of LLPCs was achieved only by combining a shot of bortezomib with maintenance therapy, e.g., cyclophosphamide, depleting the precursors of LLPCs or preventing their differentiation into LLPCs. <h3>Conclusions</h3> In lupus-prone NZB/W F1 mice, autoreactive LLPCs are generated throughout life. Their sustained therapeutic elimination requires both the depletion of LLPCs and the inhibition of their regeneration. <h3>Disclosure of Interest</h3> : None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.3408
Osseous Lesions in Urticaria Pigmentosa
Authors: Frederick G. Zak, Jerome A. Covey, John J. Snodgrass
Journal: New England Journal of Medicine (1957)

URTICARIA pigmentosa, a chronic benign cutaneous disorder occurring at all ages, is characterized clinically by pigmented macules, papules or, rarely, nodules, and microscopically by an increased number of cutaneous mast cells, the pigmentation being merely an exaggeration of the usual melanin pigment. Rubbing of the lesion may be accompanied by swelling and itching (Darier's sign).Although occasional reports, mostly in the European literature, refer to urticaria pigmentosa as a systemic disease, — for example, pseudoleukemia,1 2 3 4 5 6 7 8 9 ¶ — it was not until Ellis10 presented the autopsy findings of a child with widespread visceral involvement by mast cells that interest in the possible . . .
Abstract 4996: The VEGF quadruplex-forming sequence inhibits lung cancer cell growth
Authors: David Muench, Shelia D. Thomas, Donald M. Miller, Kara C. Sedoris
Journal: Cancer Research (2011)

Abstract Vascular endothelial growth factor (VEGF), commonly overexpressed in a variety of malignancies including lung cancer, is a key regulator of angiogenesis promoting tumor survival, growth, and metastasis. The promoters of several cancer-related genes, including VEGF, contain disproportionate sequences within nuclease hypersensitivity regions capable of forming quadruplex (four-stranded) DNA. The VEGF quadruplex-forming sequence (VEGF q), a polyG/polyC tract located in the proximal promoter region upstream of the transcription initiation site, has been implicated in the regulation of both basal and inducible VEGF expression. However, the biological role of this sequence remains unclear. We hypothesize that treatment of A549 non-small lung cancer cells with an oligonucleotide encoding VEGF q inhibits cell growth by decreasing VEGF expression and subsequent signaling through VEGF receptor 2 (FLK-1). To determine the biological role of VEGF on lung cancer cell proliferation, A549 cells were treated with VEGF q or the corresponding mutant sequence (MutVEGF), which lacks runs of two or more guanines. Our results demonstrate that VEGF q formed a parallel quadruplex structure and showed remarkable serum and intracellular stability. Confocal and flow cytometry analysis of cells treated with FITC-labeled VEGF q showed prominent uptake and nuclear/cytoplasmic localization in contrast to MutVEGF. Treatment of A549 cells with VEGF q caused a significant dose and time-dependent decrease in cell proliferation after 3 and 6 days (IC50&amp;lt;5µM) as determined by MTT assay, which was not a result of cell cycle arrest. Matrigel analysis also showed a significant reduction in tumor invasiveness after 24 h with VEGF q treatment. Although uptake of VEGF q occurred in non-transformed Hs27 human fibroblast cells, no change in cell growth was evident, indicating that the anti-proliferative effects of VEGF q are specific for malignant cells. Inhibition of cell proliferation and invasion corresponded with decreased VEGF protein expression resulting in decreased FLK-1 signaling and phosphorylation of the target proteins ERK 1/2 and AKT. These results demonstrate striking growth inhibition and decreased invasion of A549 cells in response to VEGF q related to inhibition of VEGF expression and signaling through FLK-1 and have significant therapeutic implications for the treatment of non-small cell lung cancer. 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 4996. doi:10.1158/1538-7445.AM2011-4996
OUTCOMES AND RISK FACTORS FOR RE-INTERVENTION IN CHILDREN UNDERGOING RIGHT VENTRICLE DECOMPRESSION FOR PULMONARY ATRESIA INTACT VENTRICULAR SEPTUM: RESULTS FROM A MULTI-CENTER COLLABORATIVE
Authors: Christopher J. Petit, Andrew Glatz, Athar Qureshi, Shiraz Maskatia, Ritu Sachdeva, George Nicholson, Namrita Mozumdar, Henri Justino, Wendy Whiteside, Lindsay Rogers, David Goldberg, Courtney McCracken, Michael Kelleman, Bryan Goldstein
Journal: Journal of the American College of Cardiology (2016)
Testing G-CSF responsiveness predicts the individual susceptibility to infection and consecutive treatment in recipients of high-dose chemotherapy
Authors: Christian Straka, Michael Sandherr, Hans Salwender, Hannes Wandt, Bernd Metzner, Kai Hübel, Gerda Silling, Marcus Hentrich, Daniel Franke, Rainer Schwerdtfeger, Mathias Freund, Orhan Sezer, Alexander Giagounidis, Gerhard Ehninger, Wolfgang Grimminger, Andreas Engert, Günter Schlimok, Christof Scheid, Peter Hellmann, Harald Heinisch, Hermann Einsele, Axel Hinke, Bertold Emmerich
Journal: Blood (2010)
Progress and Prospects for Human Cancer Vaccines
Authors: J S Cole, J Gruber
Journal: JNCI Journal of the National Cancer Institute (1992)

Journal Article Progress and Prospects for Human Cancer Vaccines Get access John S. Cole, John S. Cole Search for other works by this author on: Oxford Academic PubMed Google Scholar Jack Gruber Jack Gruber Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 84, Issue 1, 1 January 1992, Pages 18–23, https://doi.org/10.1093/jnci/84.1.18 Published: 01 January 1992 Article history Received: 26 June 1991 Revision received: 03 October 1991 Accepted: 15 October 1991 Published: 01 January 1992
Smoldering Acute Leukemia
Authors: Jack J. Rheingold, Richard Kaufman, Edward Adelson, Arnold Lear
Journal: New England Journal of Medicine (1963)

WE have recently seen a number of patients with acute leukemia of an atypical variety that has received little attention in the literature. These cases smolder along with low-grade clinical intensity for a period of months to years. They may continue in this fashion until death occurs from infection or other complications, or they may burst forth into a more typical picture of acute leukemia. During the smoldering phase the diagnosis may be obvious or occult. Even in the latter group, however, the diagnosis can be made if one is alert to this entity.The following cases are representative of . . .
Abstract 538: Mesenchymal stem cell subset prevents cycling of KG1a leukemic cells by cell-cell interaction
Authors: SreeKanth Donepudi,, Christopher D. Porada, Esmail Zanjani, Graça Almeida-Porada
Journal: Cancer Research (2010)

Abstract The interactions that occur between leukemic cells and the microenvironment are currently poorly understood. The definition of novel pathways that deliver survival and drug resistance signaling from the milieu to leukemic cells may lead to the discovery of new drugs that are able to target microenvironmental cues perpetuating the leukemic clones. Since the bone marrow (BM) environment is comprised of a complex assortment of different cell types, matrices and soluble and membrane-bound factors, it is crucial to start delineating specific cell-cell interactions and their effects on leukemic cell survival. Mesenchymal stem cells (MSC) are a fundamental component of the BM niche as they support hematopoiesis and are able to differentiate into neighboring cellular types. Therefore, in these studies we investigated the effect of Stro-1+ MSC on the growth and survival of KG1a, a primitive, differentiation-resistant subtype of acute myeloid leukemia. MSC and KG1a cells were co-cultured for 3 days under contact or non-contact conditions, at incremental ratios of 1:1, 1:5, 1:10 and 1:100 respectively, while maintaining a constant initial total number of cells for each dilution (n=3). In transwell non-contact cultures, KG1a cells proliferated at the same rate as KG1a alone with a 3 to 5 fold increase in cell numbers, regardless of the ratio. By contrast, when KG1a were cultured in direct contact with MSC, KG1a growth inhibition was directly proportional to the MSC:KG1a ratio. Specifically, MSC cultured with KG1a cells at ratios of 1:1, 1:5, 1:10, and 1:100 inhibited the growth of KG1a cells by 84%, 76%, 74%, and 45%, respectively while remaining 99-100% viable. Thus, we next performed cell cycle analysis using flow cytometry and found that while the cell cycle distribution of KG1a cultures were: 23% in G0/G1; 19% in G2/M; and 58% in S phase, KG1a co-cultured with MSC had undergone cell cycle arrest in S-phase (98%). Although our results contrast with prior studies showing that MSC inhibited KG1a in G1phase through the production of soluble factors, it is possible that the differences seen are due to the population of MSC used. Within the MSC, Stro-1+ cells constitute a primitive population of cells in intimate relation with the osteoblastic niche, the role of which is to retain stem cells in a quiescent state. Therefore, studies are currently underway to identify molecules responsible cell cycle arrest upon KG1a/MSC interaction. 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 538.
THU0075 The risk of venous thromboembolism in patients with rheumatoid arthritis compared to the general population: A very large cohort study
Authors: S.C. Kim, S. Schneeweiss, J. Liu, D.H. Solomon
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Some data suggest that rheumatoid arthritis (RA) is associated with an increased risk of venous thromboembolism (VTE). Prior studies have been relatively small and used a very limited set of covariates to adjust for potential confounding. <h3>Objectives</h3> To examine the risk of VTE in patients with RA compared to non-RA subjects. <h3>Methods</h3> We conducted a retrospective cohort study using health care utilization data collected by a large US commercial insurance plan. The RA cohort included adults with at least two diagnoses of RA and at least one prescription for a disease-modifying anti-rheumatic drug (DMARDs). Follow-up began with the first prescription for a DMARD, defined as the index date. Subjects who never had a diagnosis of RA were selected and matched to RA patients on age, sex, and index date with a 5:1 ratio. Patients with history of malignancy and VTE were excluded. The primary outcome was VTE, defined as the composite of deep vein thrombosis (DVT) or pulmonary embolism (PE), as a principal hospital discharge diagnosis. Incidence rates (IR) and rate ratios (RR) of VTE with 95% confidence intervals (CI) were calculated. Multivariable Cox proportional hazards models compared the risk of VTE events between RA and non-RA patients. <h3>Results</h3> The study population included 22,143 RA and 88,572 non-RA patients with a mean (SD) age of 52 (12) years with 75% women. During a mean follow-up of 2 years, 1.2% of RA patients and 0.5% non-RA patients developed VTE. The IR for VTE among RA patients was 6.1 per 1,000 person-years, 2.4 times higher (95% CI: 2.1-2.8) than the rate of non-RA patients. The IRs for both DVT (RR, 2.2, 95% CI: 1.9-2.6) and PE (RR 2.7, 95% CI: 2.2-3.5) were higher in RA patients compared with non-RA subjects. After adjusting for known risk factors of VTE, a moderately elevated risk for VTE was noted in RA (hazard ratio 1.4, 95% CI: 1.1-1.7) compared to non-RA patients. <h3>Conclusions</h3> Our results showed an increased risk of VTE, both DVT and PE, for RA patients compared with non-RA patients. The risk was attenuated but remained elevated after adjusting for known risk factors for VTE such as cardiovascular disease, surgery, hospitalization, and medications. <h3>Disclosure of Interest</h3> S. Kim Grant/Research support from: Pfizer, Takeda, S. Schneeweiss Grant/Research support from: Pfizer, Consultant for: WHISCON, RTI Health Solutions, the Lewin Group, and HealthCore, J. Liu: None Declared, D. Solomon Grant/Research support from: Amgen, Abbot, and BMS
BIOPSIA INCISIONAL ASISTIDA POR ECOENDOSCOPIA EN EL DIAGNÓSTICO HISTOLÓGICO DE LESIONES SUBEPITELIALES GASTROINTESTINALES: RESULTADOS DE UNA COHORTE PROSPECTIVA
Authors: C De La Serna Higuera, I Peñas, H Núñez, P Gil Simón, P Díez Redondo, A Vargas García, M Pérez-Miranda
Journal: Endoscopy (2013)

Introducción: Las técnicas convencionales para el diagnóstico cito-histológico de las lesiones subepiteliales gastrointestinales (LSEGI) presentan limitaciones. La PAAF por ecoendoscopia aporta escaso material, especialmente en lesiones pequeñas o de origen mesenquimal que precisan análisis inmunohistoquímico (IH). La incisión con esfinterotomo de aguja y biopsia con pinza (IEA-BP) guiada por ecoendoscopia, es una técnica de reciente desarrollo, con resultados iniciales prometedores Objetivo: Analizar las características de las LSEGI del tracto digestivo superior valorando rendimiento diagnóstico y seguridad de la IEA-BP en su estudio cito-histológico. Material y Método: Entre abril 2010- junio 2013 se recogieron prospectivamente todas las LSEGI. Se valoró morfología y vascularización con ecoendoscopio sectorial/doppler, realizándose una incisión superficial de 6 mm, con EA y potencias 30 – 60 W, introduciendose pinza convencional de biopsia, extrayéndose 3 – 5 muestras para formol. En las lesiones mesenquimales se realizó IH y determinación de índice mitótico (IM). En 8 pacientes se realizó simultáneamente PAAF-22G. Se definieron como lesiones “pequeñas”: Ø < 20 mm. Resultados: Se incluyeron 61 pacientes (V/M: 30/31). Edad media 60.05 años (22 – 89). Diámetro medio: 2.31 cm (0.65 – 9.31). Localización: Esófago/estómago/duodeno: 4/51/6. Capa: 2a/3a/4a: 5/29/27. Etiología: GIST: 21, páncreas ectópico: 11, lipoma: 7, leiomioma: 3, pólipo fibroide: 6, otras: 5, no diágnóstica: 8. Rendimiento global: 53/61: 86.88%. Lesiones pequeñas/grandes: 30/31: rendimiento pequeñas: 25/30 (83.33%): rendimiento grandes: 28/31: 90.32% (p < 0.02). La PAAF solo resultó diagnóstica en 1/8 casos (12.5%).. El análisis IH (CD 117/CD 34) fue factible en 20/21 GIST (95.23%) y para IM en 16/21 (76.19%). No existieron complicaciones. Conclusiones: La IEA-BP asistida por ecoendoscopia es una técnica segura y de alto rendimiento en el estudio de las LSEGI incluso en aquellas de menor tamaño, constituyendo una alternativa eficaz a la PAAF
Striving for Safe, Effective, Affordable Care for Cancer Survivors With Chronic Pain
Authors: Michael J. Fisch, Victor T. Chang
Journal: JAMA Oncology (2016)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Oncology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Oncology journal
MS2-3: Breast Cancer and the Environment: Developmental Reprogramming of Cancer Susceptibility by Early Life Environmental Exposures.
Authors: CL Walker
Journal: Cancer Research (2011)

Abstract In the last two decades it has become appreciated that adverse environmental exposures early in life can have a profound impact on susceptibility to adult diseases such as obesity, cardiovascular disease, diabetes, metabolic syndrome and cancer. The “developmental origins of health and disease” or DOHaD hypothesis, posits that environmental exposures during key periods of tissue development and organogenesis can “reprogram” the cell's epigenome in a way that increases susceptibility to disease later in life. It is now clear that even brief environmental exposures can reprogram developing tissues and profoundly increase risk of developing cancer in adulthood decades after the exposures occurred. This developmental reprogramming has been best appreciated in the context of early life exposures to environmental agents such as xenoestrogens that mimic steroid hormones, with such exposures dramatically increasing susceptibility to hormone-dependent tumors of the breast and reproductive tract later in life. Recent advances in the field of environmental epigenomics have provided data that epigenetic alterations in both DNA methylation and histone methyl marks are induced during developmental reprogramming. In some tissues, xenoestrogens induce these epigenetic alterations via activation of non-genomic signaling, providing a direct link between xenoestrogen exposure and disruption of the cell's epigenetic machinery. For example, xenoestrogeninduced activation of non-genomic PI3K/AKT signaling has been shown to target the histone methyltransferase EZH2, modulating the activity of this epigenetic “writer” and disrupting the proper “installation” of epigenetic histone methyl marks during development. Understanding the nature of the epigenetic reprogramming induced by early life exposures to xenoestrogens (and other environmental agents) has important implications for our understanding of breast cancer susceptibility across the life-course and for identifying effective strategies to prevent this disease. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr MS2-3.
Bone SPECT Findings in Runner’s Knee
Authors: AMJA VAN DEN EECKHAUT, NATASCHA WALGRAEVE, FRANK DE GEETER
Journal: Clinical Nuclear Medicine (2003)

VAN DEN EECKHAUT, AMJA M.D.; WALGRAEVE, NATASCHA M.D.; DE GEETER, FRANK M.D., PH.D. Author Information
Exercise-induced ischemic colitis in an amateur marathon runner
Authors: Amine Benmassaoud, Yonca Kanber, Josiane Nawar, Talat Bessissow
Journal: Endoscopy (2014)

A previously healthy 25-year-old man presented to the emergency department with acute-onset diffuse abdominal pain, which started halfway through a marathon run. Soon after presentation, he had a small amount of coffee-ground emesis and 10 – 15 loose bowel movements with hematochezia. His abdomen was diffusely tender to mild palpation. Laboratory investigation revealed leukocytosis, mild acute kidney injury, and rhabdomyolysis. Stool cultures for bacteria, ova and parasite, and Clostridium difficile were negative.
Regional Radioactivity Discrepancy Between Tc-99m GSA and Tc-99m Phytate Liver Scans in a Patient with Massive Hepatic Necrosis
Authors: Shiro Akaki, Mototsugu Saeki, Toshihiro Iguchi, Yoshihiro Okumura, Shuhei Sato, Masahiro Kuroda, Susumu Kanazawa, Yoshio Hiraki, Toshio Uraoka, Nobuyuki Baba, Kosaku Sakaguchi
Journal: Clinical Nuclear Medicine (2002)

A 22-year-old woman with severe acute hepatitis underwent a Tc-99m galactosyl human serum albumin (GSA) scan. Intense accumulation was observed in the cephalic region of the right hepatic lobe, whereas the accumulation was reduced in the left lobe and the caudal region of the right lobe. A computed tomographic (CT) scan showed that the left lobe and the caudal region of the right posterior segment had atrophied and become hypodense, which were thought to represent postnecrotic scarring after massive hepatic necrosis. The relatively hyperdense region in the right lobe was slightly swollen and was thought to represent regenerating liver tissue or a “potato liver.” Compared with the CT, the regions of elevated Tc-99m GSA accumulation correlated well with the areas of regenerating liver tissue, and the regions with reduced accumulation corresponded closely with the areas of postnecrotic scarring. On a Tc-99m phytate scan, unlike the Tc-99m GSA scan, the radiocolloid accumulation was intense in the left lobe and caudal region of the right lobe and reduced in the cephalic region of the right lobe. Together, the Tc-99m GSA scan and the Tc-99m phytate scan formed a set of exact “nega-posi” images. Biopsy specimens obtained during laparoscopy showed a few hepatocyte columns in the postnecrotic scarred left lobe. Severe disruption of the hepatocytes, prominent inflammatory cell infiltration, and obvious Kupffer cell hypertrophy and clustering were also observed.