tbuckley/cabot-search huggingface dataset:
Abstract P264: Healthy dietary interventions and Lipoprotein (a) plasma levels: Results from the Omni Heart Trial
Authors: Bernhard Haring, Moritz C Wyler von Ballmoos, Lawrence J Appel, Frank M Sacks
Journal: Circulation (2014)

Background: Increased lipoprotein (a) [Lp(a)] levels are associated with atherosclerotic cardiovascular disease. Plasma Lp(a) levels are mainly genetically determined by race with levels higher in blacks compared to whites. Dietary interventions have been reported to alter Lp(a) but evidence is sparse. No study has evaluated the effect of macronutrient composition on Lp(a) concentration and racial differences. Objective: To compare three healthy, DASH-style dietary interventions differing in macronutrient content on the effect on Lp(a) concentrations in blacks and whites. Design: Secondary analysis of a randomized, 3-period feeding study including 152 (88 blacks/64 whites) individuals. Participants were given DASH-type healthy diets rich in carbohydrates [Carb], in protein [Prot] or in unsaturated fat [Unsat Fat] for 6 weeks each. Plasma Lp(a) concentration was assessed at baseline and after each intervention. Results: At baseline, median Lp(a) plasma level was 18 mg/dl overall, 9 mg/dl in whites and 28.5mg/dl in blacks. The Unsat Fat diet lowered Lp(a) by 1.2mg/dl (95% CI, -0.3,-2.2; p= 0.015) compared with the Carb diet, and by 2.7 mg/dl (95% CI, -1.7,-3.7; p&lt;0.001) compared with the Prot diet (Table). The effects on Lp(a) of the controlled diets tended to be greater in blacks than whites, especially the reduction in Lp(a) on the Unsat compared to the Prot diet (-3.7 in blacks vs. -1.0 mg/dl in whites, P=0.008). On self-selected diet (prior to feeding) or intervention diets, blacks had higher mean Lp(a) than did whites. Conclusions: Compared to diets rich in carbohydrate or protein, a DASH-type diet high in unsaturated fat lowered Lp(a). These changes were greater in blacks compared to whites. Our results highlight a potential means to reduce racial disparities in CVD. Table: Differences in Lp(a) concentration (mg/dl) between study diets by ethnicity
Abstract 426: Transcriptional regulation of dnmt1 by E2F1 in melanoma progression
Authors: CAMILA T. DA SILVA, Fernanda Molognoni, Fabiana H. M. de Melo, Miriam Galvonas Jasiulionis
Journal: Cancer Research (2014)

Abstract Melanoma is the most aggressive skin cancer due to its high resistance to currently available therapy. Like other kinds of cancer, melanoma presents changes in DNA methylation and epigenetic machinery such as Dnmt1, however it is still unclear why tumor cells acquire these epigenetic alterations. The aim of this study was to analyze the mechanisms involved in Dnmt1 transcriptional regulation by the transcription factor E2F1 in melanoma progression. The cell model used in this study was previously developed in our laboratory, submitting non-tumorigenic murine melanocytes (melan-a) to successive cycles of anchorage blockade. A linear cell model for melanoma was obtained consisting in pre-malignant (1C and 4C), tumorigenic non-metastatic (4C11-) and metastatic (4C11+) cell lines. Bioinformatics data show the existence of four transcripts for Dnmt1 in mice. The transcripts 1 and 2 have the same promoter, and the transcripts 3 and 4 share a different promoter. Real time PCR showed the absence of transcript 3 in all cell lines analyzed. The transcript 4 was present in all lineages, but no significant change in its expression was observed in any one compared to melan- a melanocytes. Transcripts 1 and 2 are present and their levels are increased in 1C, 4C, 4C11- and 4C11+ compared to melan-a cells. Chromatin immunoprecipitation (ChIP) showed increased binding of E2F1 in Dnmt1 promoter in 1C, 4C, 4C11- and 4C11+ compared to melan-a cells. Interestingly, the intensity of binding was stronger in the first promoter, which regulates transcripts 1 and 2, than in the second promoter, which regulates transcripts 3 and 4. These results show for the first time that E2F1 may have an important role in the transcription regulation of Dnmt1 during melanoma progression. Additionally, we observed the increase in superoxide anion (O2.-) in 1C compared to melan-a cells. Recently published data from our group showed that depleting O2.- with MnTBAP scavenger during melan-a anchorage blockade cycles, the malignant transformation is drastically compromised. Here, we showed that 1C cells treated with MnTBAP do not have Dnmt1 mRNA and protein increase compared to melan-a cells. Furthermore, E2F1 levels seem to be regulated by O2.- in 1C cells, indicating that O2.- can be a possible mediator for E2F1 regulation and Dnmt1 transcriptional regulation in melanoma progression. Together, these data suggest an important role of oxidative stress and epigenetic mechanisms in the first steps of melanoma progression. Supported by FAPESP and CNPq. Citation Format: CAMILA T. DA SILVA, Fernanda Molognoni, Fabiana H. M. de Melo, Miriam Galvonas Jasiulionis. Transcriptional regulation of dnmt1 by E2F1 in melanoma progression. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 426. doi:10.1158/1538-7445.AM2014-426
Updated analysis of a phase II study (20060314) of panitumumab (pmab) with FOLFIRI as first-line treatment of patients (pts) with metastatic colorectal cancer (mCRC)
Authors: R. Greil, H. Letocha, E. Gamelin, J. Thaler, R. Hofheinz, L. Mineur, E. Fernebro, M. Karthaus, L. Wright, C. Köhne
Journal: Journal of Clinical Oncology (2009)

4085 Background: The fully human anti-epidermal growth factor receptor monoclonal antibody pmab, has proven monotherapy activity in chemotherapy refractory mCRC pts with wild-type KRAS-expressing tumors. This first-line, single-arm phase II study is prospectively evaluating whether KRAS status predicts response to treatment when pmab is combined with FOLFIRI. Methods: In this ongoing study, pts with histologically confirmed mCRC (no prior systemic treatment) and ECOG PS 0–2 were enrolled at 36 sites across Europe. Pmab (6mg/kg) and FOLFIRI are administered every 2 weeks. The primary endpoint is objective response rate; secondary endpoints include disease control rate, duration of response, time to response, progression-free survival, time to progression and safety. Results: Data cut-off for the initial interim analysis was 27 June 08 and pending approval of protocol amendment 2, the cut off date for 16 week response rate is 15 Oct 08. Of the 154 pts enrolled, 68% are male; median age is 64 yrs (range, 21–84) and the majority (95%) of pts had ECOG PS 0–1. All pts have received at least one cycle of study treatment; 18% of pts have received ≤2 cycles of full combination therapy and the median number of cycles received is 6. At time of data cut-off, 112 patients (73%) were still receiving at least one element of combination therapy and 29% had stopped treatment with pmab. The most common reason for discontinuing treatment was disease progression (10%). Median follow-up time was 14.3 weeks for all enrolled pts. A total of 97% of patients had experienced at least one adverse event (any grade) and 55% of patients had experienced a grade 3/4 adverse event. There were four reported grade 5 events (hematemesis, rectal hemorrhage, vena cava thrombosis, general physical health deterioration). At time of interim analysis, tissue samples for KRAS analysis are available for approximately 80% of patients. Conclusions: Combining pmab with FOLFIRI in the first-line setting appears to be a well-tolerated regimen. Response rate at 16 weeks in the overall population and by KRAS status and updated safety will be presented. [Table: see text]
Making a Difference in Africa
Authors: Rebecca Voelker
Journal: JAMA (1999)

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 HomeNew OnlineCurrent IssueFor Authors 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Abstract 329: Six at Six: Interleukin-6 Measured at 6 Hours After Cardiac Arrest Is a Good Predictive Biomarker of Outcome of Post--Cardiac Arrest Syndrome in Humans
Authors: Koichiro Shinozaki, Lance B Becker, Shigeto Oda, Hiroyuki Hirasawa
Journal: Circulation (2014)

Introduction: As early as 3h after cardiac arrest (CA), the blood level of various cytokines increases and may be associated with outcome of post cardiac arrest syndrome (PCAS). However, it remains uncertain whether blood levels of these cytokines including IL-6 have significance as predictors of outcome following cardiac arrest. Objective: To demonstrate any association between circulating IL-6 level, one of major pro-inflammatory cytokines, and mortality in PCAS of humans. Methods: This was a multicenter observational study conducted between 2006-09 in Chiba, Japan, involving non-trauma CA adult patients. All patients admitted to acute care units were included. Patient characteristics were extracted following an Utstein template. The primary outcome was mortality through the end of the study. IL-6 blood levels were measured on admission, at 6hr, and 24hr after CA. Patients were classified into three groups (high, middle, and low) according to IL-6 levels at each time point. We evaluated the association of IL-6 levels with survival using the Kaplan-Meier method. A Cox proportional hazard model with a step-wise selection procedure was used to identify independent variables associated with overall survival. Results: A total of 227 patients were included in this study. Survival time in “High IL-6” group was shorter than “Low” group. There were significant differences in blood level of IL-6 in the three groups, high (&gt;811pg/mL), mid (811-93pg/mL), and low (&lt;93pg/mL), only at 6hr (long rank; high vs. low p&lt;0.001, high vs. mid p=0.07, and mid vs. low p=0.001 on admission; p&lt;0.001, p&lt;0.001, and p&lt;0.001 at 6hr, respectively; p&lt;0.001, p&lt;0.001, and p=0.936 at 24hr, respectively). Three factors were identified as independent predictors of early death; no bystander CPR (hazard ratio [95% confidential interval], 2.59 [1.10-6.10], p=0.03), a lack of therapeutic hypothermia (2.68 [1.70-4.22], p&lt;0.001), and IL-6 levels at 6hr (high, reference; mid, 0.41 [0.25-0.66], p&lt;0.001; low, 0.11 [0.06-0.20], p&lt;0.001). Conclusions: IL-6 measured at 6hr can predict mortality. It should be studied further to see if it can help direct therapeutic decision-making and whether it can define optimal populations for study in clinical trials.
THE ACUTE-PHASE RESPONSE IN (NZB X NZW)F1 AND MRL/1 MICE - CONTRASTING PATTERNS RESEMBLING THOSE IN HUMAN SYSTEMIC LUPUS-ERYTHEMATOSUS AND RHEUMATOID-ARTHRITIS, RESPECTIVELY
Authors: C Rordorf, Hp Schnebli, Ml Baltz, Ga Tennent, Mb Pepys
Journal: The Journal of Experimental Medicine (1982)
Assessing the educational component of pulmonary rehabilitation with the lung information needs questionnaire (LINQ)
Authors: Ria Fowler, Karen Ingram, Claire Nolan, Pippa Marns, Amy Clark, Michael Polkey, William Man
Journal: European Respiratory Journal (2011)

Introduction:  Educational sessions are an integral part of pulmonary rehabilitation (PR) programs but there are few tools to assess their impact. The Lung Information Needs Questionnaire (LINQ) is patient reported and designed to assess the information needed to understand lung diseases and to maximise self-management skills (Hyland et al 2006). A decreased score indicates less information requirements. We hypothesised that the LINQ is sensitive to change after a PR program and provides additional information to tests of exercise capacity and health status.   Method:  We prospectively measured the LINQ, the self-report Chronic Respiratory Disease Questionnaire (CRDQ-SR), Hospital Anxiety & Depression score (HAD) and incremental shuttle walk (ISW) in 217 patients before and after an 8-week outpatient PR program. 11 patients, who declined the outpatient PR program and were prescribed a home exercise program (HE), acted as controls. Mean LINQ pre- and post- PR was compared with paired t-test, and unpaired t-test was used to compare mean LINQ changes following PR and HE. Pearson9s correlation was used to examine relationship between changes in LINQ and other outcome measures.   Results:  All 217 patients completed LINQ pre- and post-PR. Mean LINQ fell significantly after PR (95% CI -3.8 to -4.9; p   Conclusion:  The LINQ is sensitive to change after PR, provides additional information to conventional outcome measures and may be useful to assess the educational component of PR programs.
A Randomized Trial of a Schlemm's Canal Microstent with Phacoemulsification for Reducing Intraocular Pressure in Open-Angle Glaucoma
Authors: Norbert Pfeiffer, Julian Garcia-Feijoo, Jose M. Martinez-de-la-Casa, Jose M. Larrosa, Antonio Fea, Hans Lemij, Stefano Gandolfi, Oliver Schwenn, Katrin Lorenz, Thomas W. Samuelson
Journal: Ophthalmology (2015)
Chronic staphylococcal scalded skin syndrome
Authors: None Shelley, None Shelley, None Talanin
Journal: British Journal of Dermatology (1998)

Staphylococcal scalded skin syndrome (SSSS), not previously recorded as a chronic disease, persisted for 2 years in a 50‐year‐old woman with epilepsy and cerebellar ataxia. Lesions initially suggestive of erythema multiforme and toxic epidermal necrolysis evolved over 2 years into those typical for SSSS, with extensive erosions and subcorneal blisters, showing an epidermal split at the granular cell layer. Exfoliatin A‐producing phage I‐III Staphylococcus aureus, previously linked only to acute mild adult cases of SSSS, was cultured from purulent discharge in the patient's eyes, ears and open skin lesions. The roles of epilepsy and antiepileptic medications are discussed as possible predisposing factors.
Pyoderma gangrenosum associated with Takayasu's arteritis responding to cyclosporin
Authors: None Fearfield, None Ross, None Farrell, None Costello, None Bunker, None Staughton
Journal: British Journal of Dermatology (1999)

A 33‐year‐old caucasian woman with pyoderma gangrenosum associated with Takayasu's arteritis responded to treatment with cyclosporin. This patient is unusual in that both ulcerative and vesiculopustular forms of pyoderma gangrenosum were present. This has not previously been reported with Takayasu's arteritis.
Lead Extraction in the Contemporary Setting: The LExICon Study
Authors: Oussama Wazni, Laurence M. Epstein, Roger G. Carrillo, Charles Love, Stuart W. Adler, David W. Riggio, Shahzad S. Karim, Jamil Bashir, Arnold J. Greenspon, John P. DiMarco, Joshua M. Cooper, John R. Onufer, Kenneth A. Ellenbogen, Stephen P. Kutalek, Sherri Dentry-Mabry, Carolyn M. Ervin, Bruce L. Wilkoff
Journal: Journal of the American College of Cardiology (2010)
Close collaboration between academia, industry and drug regulators is required in the development of allergen products for specific immunotherapy in children
Authors: I. Eichler, E. Sala Soriano
Journal: Allergy (2011)

Modification of the response to allergens at an early stage and thereby of the natural history of a respiratory allergic disease by preventing disease progression would constitute the key benefit of specific immunotherapy (SIT) in children. However, although allergen products for SIT have been on the market on a named-patient basis for many years, long-term efficacy, the optimal duration of the treatment and the optimal dosage have not been sufficiently elaborated until now. The enactment of the Therapy Allergen Ordinance in Germany mandates that allergen products for SIT of the most prevalent allergies must submit an application for marketing authorization to the German authorities. In line with the European Paediatric Regulation, decisions by the European Medicines Agency on agreed paediatric investigation plans must be included in these applications. These regulatory requirements provide a unique opportunity to fill the gap in knowledge concerning the benefits of SIT for children and to obtain the data needed to support evidence-based authorization of allergen products for immunotherapy. This goal can only be achieved through close cooperation between academia, drug regulators and industry as well as parent/patient organizations.
C3a and C5a Stimulate Chemotaxis of Human Mast Cells
Authors: Karin Hartmann, Beate M. Henz, Sabine Krüger-Krasagakes, Jörg Köhl, Reinhard Burger, Sven Guhl, Ingo Haase, Undine Lippert, Torsten Zuberbier
Journal: Blood (1997)
Abstract 275: Burkitt lymphoma cells express GLI1 but are not responsive to Hedgehog signaling
Authors: Joon Won Yoon, Marisa Gallant, Marilynn Lamm, King-Fu Leong, Philip Iannaccone, David O. Walterhouse
Journal: Cancer Research (2011)

Abstract Activation of the Hedgehog (HH) signaling pathway has been associated with a wide variety of human cancers. Some B-cell lymphomas express components of the HH signaling pathway, including patched (PTCH), smoothened (SMO), and GLI1. There is also evidence that HH ligands function as survival factors in these malignancies. However, specific roles for HH signaling in Burkitt lymphoma have not been characterized. Previously we showed that constitutive expression of c-MYC in Burkitt lymphoma cells up-regulates GLI1 and that GLI1 functions as an anti-apoptotic factor in this setting. Similar to other B-cell malignancies, we have shown expression of PTCH, SMO, and GLI1 in five Burkitt lymphoma cells lines. To test the role of HH signaling in Burkitt lymphoma, we exposed the cells to Sonic Hedgehog peptide or to SHH-containing conditioned media and measured the level of PTCH and GLI1 mRNA expression by quantitative RT PCR; cell viability by MTT assay; cell proliferation by BrdU incorporation; and apoptosis by caspase 3/7 assay. Although control cells (MC3T3) showed dramatic up-regulation of GLI1 and PTCH expression, the Burkitt lymphoma cell lines did not show changes in any of the assays. To inhibit HH signaling, we treated the Burkitt lymphoma cells with the SMO inhibitor, cyclopamine. Cyclopamine treatment did not affect GLI1 expression measured by quantitative RT PCR. Cyclopamine reduced viability of Burkitt lymphoma cells measured by MTT assays only when used at high concentrations (&amp;gt;5 µm), possibly representing a non-specific cytotoxic effect. Collectively, the results suggest that Burkitt lymphoma cells are not HH responsive and that constitutive c-MYC expression plays an important role in regulating GLI1 expression. 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 275. doi:10.1158/1538-7445.AM2011-275
Nucleoside analogue 9-β-D-arabinofuranosyl-2-fluoroadenine (Fara-A) inhibits VEGF expression through HIF-1α expresssion in ovarian cancer cells
Authors: Bing-Hua Jiang, Jing Fang, Eddie Reed
Journal: Cancer Research (2004)

Proc Amer Assoc Cancer Res, Volume 45, 2004

2970 

Angiogenesis is a complex process by which new blood vessels arise from the pre-existing vasculature. Vascular endothelial growth factor (VEGF), also known as vascular permeability factor (VPF), is important for tumor progression and angiogenesis, and is a negative clinical prognostic factor in ovarian cancer. 9-β-D-arabinofuranosyl-2-fluoroadenine (Fara-A), the nucleoside of the therapeutic agent, interferes with DNA replication and repair and induces apoptosis of cancer cells. However, the molecular mechanism of its action is not completely understood. Here we showed that VEGF mRNA and protein expression in ovarian cancer cells was inhibited by Fara-A. To understand the mechanism of VEGF expression inhibited by Fara-A, we used VEGF reporter containing human VEGF promoter, and found that Fara-A inhibited the VEGF reporter activity in a dose-dependent manner in the ovarian cancer cells. This result indicated that VEGF transcriptional activation was inhibited by Fara-A. In response to hypoxia, VEGF gene transcription is mediated by the hypoxia-inducible factor-1 (HIF-1). HIF-1 is composed of HIF-1α and HIF-1β subunits. HIF-1 activity is mainly regulated through the level of HIF-1α expression in the cells. To determine whether Fara-A inhibited transcriptional activation of VEGF through HIF-1, we found that Fara-A dramatically inhibited levels of HIF-1α protein, but not HIF-1β protein. To study the signaling pathways involved in the process, we found that Fara-A inhibited phosphatidylinositol 3-kinase (PI3K) signaling. Fara-A inhibited the phosphorylation of AKT in the cells. Over-expression of active form of AKT restored Fara-A-inhibited VEGF transcriptional activation in a dose-dependent manner, suggesting that Fara-A inhibits VEGF and HIF-1 expression through PI3K/AKT signaling. Taken together, we showed that Fara-A inhibits VEGF expression through the transcriptional activation and HIF-1α expression, which is regulated by PI3K/AKT signaling in the ovarian cancer cells.