tbuckley/cabot-search huggingface dataset:
Efficacy of Blended Cognitive Behavior Therapy for High Fear of Recurrence in Breast, Prostate, and Colorectal Cancer Survivors: The SWORD Study, a Randomized Controlled Trial
Authors: Marieke van de Wal, Belinda Thewes, Marieke Gielissen, Anne Speckens, Judith Prins
Journal: Journal of Clinical Oncology (2017)

Purpose Fear of cancer recurrence (FCR) is a common problem experienced by cancer survivors. Approximately one third of survivors report high FCR. This study aimed to evaluate whether blended cognitive behavior therapy (bCBT) can reduce the severity of FCR in cancer survivors curatively treated for breast, prostate, or colorectal cancer. Patients and Methods This randomized controlled trial included 88 cancer survivors with high FCR (Cancer Worry Scale score ≥ 14) from 6 months to 5 years after cancer treatment. Participants were randomly allocated (ratio 1:1, stratified by cancer type) to receive bCBT, including five face-to face and three online sessions (n = 45) or care as usual (CAU; n = 43). Participants completed questionnaires at baseline (T0) and 3 months later (T1). The intervention group completed bCBT between T0 and T1. The primary outcome was FCR severity assessed with the Cancer Worry Scale. Secondary outcomes included other distress-related measures. Statistical (one-way between-group analyses of covariance) and clinical effects (clinically significant improvement) were analyzed by intention to treat. Results Participants who received bCBT reported significantly less FCR than those who received CAU (mean difference, -3.48; 95% CI, -4.69 to -2.28; P < .001) with a moderate-to-large effect size ( d = 0.76). Clinically significant improvement in FCR was significantly higher in the bCBT group than in the CAU group (13 [29%] of 45 compared with 0 [0%] of 43; P < .001); self-rated improvement was also higher in the bCBT group (30 [71%] of 42 compared with 12 [32%] of 38 in the CAU group; P < .001). Conclusion bCBT has a statistically and clinically significant effect on the severity of FCR in cancer survivors and is a promising new treatment approach.
Dog Exposure During the First Year of Life and Type 1 Diabetes in Childhood
Authors: Mona-Lisa Wernroth, Bodil Svennblad, Katja Fall, Fang Fang, Catarina Almqvist, Tove Fall
Journal: JAMA Pediatrics (2017)

The association between early exposure to animals and type 1 diabetes in childhood is not clear.To determine whether exposure to dogs during the first year of life is associated with the development of type 1 diabetes in childhood.A nationwide cohort study utilizing high-quality Swedish national demographic and health registers was conducted. A total of 840 593 children born in Sweden from January 1, 2001, to December 31, 2010, were evaluated. Type 1 diabetes was identified using diagnosis codes from hospitals and dispensed prescriptions of insulin. Cox proportional hazards regression models were used to assess the association between exposure to dogs and risk of type 1 diabetes in childhood. The possible association was further investigated by performing dose-response and breed group-specific analyses. The cohort was followed up until September 30, 2012. Data analysis was conducted from October 15, 2015, to February 8, 2017.Having a parent who was registered as a dog owner during the child's first year of life.Childhood-onset type 1 diabetes.Of the 840 593 children reviewed, 408 272 (48.6%) were girls; mean (SD) age at diagnosis of type 1 diabetes was 5.1 (2.6) years. Dog exposure was identified in 102 035 children (12.1%). Follow-up started at age 1 year, and the children were followed up for as long as 10.7 years (median, 5.5 years). During follow-up, 1999 children developed type 1 diabetes. No association was found between exposure to dogs (adjusted hazard ratio [HR], 1.00; 95% CI, 0.86-1.16) and type 1 diabetes in childhood. The size of the dog (adjusted HR per 10-cm increase in height, 0.96; 95% CI, 0.86-1.06) or number of dogs in the household (1 dog: adjusted HR, 1.07; 95% CI, 0.91-1.26; 2 dogs: 0.79; 95% CI, 0.54-1.15; ≥3 dogs: 0.50; 95% CI, 0.23-1.12; compared with nonexposed children) also was not associated with type 1 diabetes risk. An analysis of children whose parent had type 1 diabetes (210 events) yielded an adjusted HR of 0.71 (95% CI, 0.43-1.17) for dog exposure.In a nationwide study, no evidence supporting an association of register-derived measures of dog exposure with childhood type 1 diabetes was identified.
Proposed Definition of Necrotizing Enterocolitis May Be of Limited Value
Authors: Jeffrey D. Horbar, Roger F. Soll, Erika M. Edwards
Journal: JAMA Pediatrics (2017)

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 Pediatrics 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 Pediatrics journal
Abnormal Heavy/Light Chain Ratio after Treatment Is a Robust Predictor of Shorter Survival in Patients with IgA Myeloma
Authors: Yoshiaki Abe, Yasuhito Suehara, Hiroyuki Takamatsu, Yoshiaki Usui, Kentaro Narita, Masami Takeuchi, Kelly Endean, Kosei Matsue
Journal: Blood (2016)
Glucocorticoids in rheumatoid arthritis: the picture is shaping up
Authors: Frank Buttgereit, Johannes W Bijlsma
Journal: Annals of the Rheumatic Diseases (2017)

Despite the well-known efficacy of glucocorticoids (GCs), it is more common than exceptional that their known adverse event profile and co-morbidity implications elicit fierce debates when discussing their benefit–risk profile. These discussions usually come up, especially among GC ‘supporters’ and ‘opponents’,1 when trying to elaborate recommendations on how to use these drugs best in the treatment of rheumatic diseases such as rheumatoid arthritis (RA),2 polymyalgia rheumatica,3 giant cell arteritis,4 systemic lupus erythematodes,5 6 myositis7 and even systemic sclerosis.7 For example, very divergent opinions were learnt during work on the European League Against Rheumatism (EULAR) recommendations (2013 update) for the management of RA.2 As a result, only 73% (the lowest majority level of all recommendations) of the members approved the suggestion that GCs should only be used as bridging therapy for up to 6 months, ideally tapering them at earlier time points. Interestingly, when looking at the members voting against it, about half of them thought the statement was too weak, whereas the other half considered it to be too strong.2 Nevertheless, the level of agreement (strength of recommendation) was quite high (mean of 8.9) on final anonymous grading. It should also be noted that the group did not explicitly discuss the chronic use of GC in established RA.

Indeed, many patients and quite some physicians are still uncertain about the actual benefit:risk ratio of GCs.1 This uncertainty might prevent optimal treatment under conditions where GC treatment is known to be of added value. Fortunately, our view on the most optimal use of these drugs does slowly but constantly maturate. This primarily results from thorough analyses of accumulated data in order to update recommendations, but there are also new and often qualitatively better data coming in to enrich our knowledge. A …
Nonalcoholic Fatty Liver Disease and Subclinical Atherosclerosis: Analyses from the Coronary Artery Risk Development in Young Adults (CARDIA) Study
Authors: Lisa B. VanWagner, Christina M. Shay, Hongyan Ning, John Wilkins, Cora E. Lewis, Jeff Carr, James G. Terry, Donald Lloyd-Jones, David Jacobs, Mercedes Carnethon
Journal: Circulation (2013)

Background: Nonalcoholic Fatty Liver Disease (NAFLD) and excess visceral adipose tissue (VAT) are associated with cardiovascular disease (CVD). Recent studies suggest that NAFLD and coronary artery calcification (CAC) are related independent of VAT. In a population-based cross-sectional sample of black and white adults free from prevalent liver or heart disease, we tested the hypothesis that NAFLD is associated with the presence of CAC and abdominal aortoiliac calcification (AAC) independent of VAT and other CVD risk factors. Methods: Participants from the Coronary Artery Risk Development in Young Adults study (Y25 exam) with concurrent computed tomography quantification of liver fat, CAC and AAC were included (n=2,163). NAFLD was defined as liver attenuation ≤ 40 Hounsfield Units after exclusion of other causes of liver fat (medication/alcohol use). Using the Agatston method, CAC/AAC presence was defined as a score > 0. Logistic regression models were used to calculate odds ratios and 95% confidence inte...
Updated molecular analyses of exons 19 and 21 of the epidermal growth factor receptor (<i>EGFR</i>) gene and codons 12 and 13 of the <i>KRAS</i> gene in non-small cell lung cancer (NSCLC) patients treated with erlotinib in National Cancer Institute of Cancer
Authors: F. A. Shepherd, K. Ding, A. Sakurada, G. Da Cunha Santos, C. Zhu, L. Seymour, M. Whitehead, S. Kamel-Reid, J. Squire, M. S. Tsao
Journal: Journal of Clinical Oncology (2007)

7571 Background: BR.21 demonstrated significant survival benefit from erlotinib for NSCLC patients (Shepherd, NEJM 2005). EGFR gene point mutations in exon 21 and deletions in exon 19 predict response to EGFR TKIs, but the predictive value of EGFR mutations (Mut) or high copy number (Amp) on survival remains unclear. Methods: The sensitivity of PCR-sequencing to detect EGFR mutations may be suboptimal. Thus, we re-analyzed all BR.21 samples with available material using a fluourescent-based PCR technique (Pan, JMD 2005;7:396) and ScorpionIM kits (DxS, Manchester, UK) as they may detect mutations in samples with only 5–10% tumor DNA. 204 samples were analyzed successfully for EGFR Mut, 206 for KRAS Mut and 159 by FISH for EGFR Amp. Results: Exon 19 deletion and/or exon 21 L858R Mut were identified in 34 patients (overall Mut rate 17%). EGFR high polysomy or true amplification was present in 61 patients (38%), and 30 patients (15%) had KRAS Mut. Overall response rates were EGFR wildtype (WT)/Mut: 7%/27%, p=0.03; KRAS WT/Mut: 10%/5%, p=0.69; No Amp/Amp: 5%/21%, p=0.02. Hazard ratios for survival benefit were EGFR WT: 0.74 (0.52–1.05, p=0.09), Mut: 0.55 (0.25–1.19, p=0.12); KRAS WT: 0.69 (0.9–0.97, p=0.03), Mut: 1.67 (0.62–4.50, p=0.31); no Amp: 0.80 (0.49–1.29, p=0.35), Amp: 0.43 0.23–0.78, p=0.004). The test for interaction was borderline for KRAS Mut (0.09) but was not significant for EGFR Mut (p=0.47) or EGFR Amp (0.12). It was significant only for non-smokers with EGFR Amp (p=0.04). In the multiple Cox regression model, including all markers, EGFR Amp was both prognostic for poorer survival (p=0.005) and predictive of a differential survival benefit from erlotinib (p=0.009). EGFR and KRAS Mut were not significant prognostic or predictive markers. Conclusion: EGFR genotype and copy number are predictive of objective response to erlotinib. In BR.21, EGFR gene copy number is the strongest molecular prognostic marker and the only significant molecular predictor of a differential survival benefit from treatment. [Table: see text]
HEREDITARY FIBRINOGEN A alpha-CHAIN AMYLOIDOSIS: PHENOTYPIC CHARACTERIZATION AND THE ROLE OF LIVER TRANSPLANTATION
Authors: Arie J. Stangou, Nicholas R. Banner, Mohamed Rela, Bernard C. Portmann, Julia Wendon, Elizabeth Sizer, Michael A. Heneghan, Muriel Buxton-Thomas, Mark Monaghan, Christopher J. Mathias, Bruce Hendry, Juris J. Liepnieks, John G. O'Grady, Merrill D. Bensons, Nigel Heaton
Journal: Hepatology (2008)
Lipid peroxidation: Its effects on the formulation and use of pharmaceutical emulsions
Authors: Ramona Khanum, Haema Thevanayagam
Journal: Asian Journal of Pharmaceutical Sciences (2017)

Pharmaceutical delivery systems are developed to improve the physicochemical properties of therapeutic compounds. Emulsions are one of these drug delivering systems formulated using water, oils and lipids as main ingredients. Extensive data are usually generated on the physical and chemical characteristics of these oil-in-water and lipid emulsions. However, the oxidative tendency of emulsions is often overlooked. Oxidation impacts the overall quality and safety of these pharmaceutical emulsions. Additionally, introducing oxidatively unstable emulsions into biological systems further promotes oxidation in situ. Products of these reactions then continue to pose serious harm to cells and fuel other physiological oxidation reactions. Consequently, the increase of oxidation products leads to oxidative damage to biological systems. Thus, emulsions with lower lipid peroxidation are more stable and will reduce the negative effects of oxidation in situ. Preventive measures during the formulation of emulsions are important. Many naturally occurring and cost effective substances possess low oxidation tendencies and confer oxidative protection when used in emulsions. Additionally, certain preparatory methods should be employed to reduce or better control lipid peroxidation. Finally, emulsions must be evaluated for their oxidation susceptibility using the various techniques available. Careful attention to the preparation of emulsions and assessment of their oxidative stability will help produce safer emulsions without compromising efficacy.
Increasing Diversity in Dermatology Residencies
Authors: Ajay Kailas, Darrell S. Rigel
Journal: JAMA Dermatology (2017)

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 Dermatology 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 Dermatology journal
Selective testing for calreticulin gene mutations in patients with splanchnic vein thrombosis: A prospective cohort study
Authors: Johanne Poisson, Aurélie Plessier, Jean-Jacques Kiladjian, Fanny Turon, Bruno Cassinat, Annalisa Andreoli, Emmanuelle De Raucourt, Odile Goria, Kamal Zekrini, Christophe Bureau, Florence Lorre, Francisco Cervantes, Dolors Colomer, François Durand, Juan-Carlos Garcia-Pagan, Nicole Casadevall, Dominique-Charles Valla, Pierre-Emmanuel Rautou, Christophe Marzac
Journal: Journal of Hepatology (2017)
Erratum: Frequent loss of heterozygosity at 7q31.1 is associated with tumor aggressiveness and progression (Cancer Research (September 15, 1995) 55 (4114-4119))
Authors: S. Takahashi, A. L. Shan, S. R. Ritland, K. A. Delacey, D. G. Bostwick, M. M. Lieber, Stephen N Thibodeau, Robert Brian Jenkins
Journal: Cancer Research (1996)
Reverse sphincterotomy of the minor papilla via the major papilla for chronic pancreatitis with incomplete pancreas divisum
Authors: Radhika Chavan, Rakesh Kalapala, Zaheer Nabi, Sundeep Lakhtakia, D. Reddy
Journal: Endoscopy (2017)

A 35-year-old man presented with recurrent abdominal pain due to chronic alcoholic pancreatitis. Magnetic resonance cholangiopancreatography showed a dilated tortuous main pancreatic duct with incomplete pancreas divisum.
Expression of cytokines in the vitreous of a uveal melanoma animal model
Authors: Amanda L. Caissie, João P. Souza Filho, Jean-Claude A. Marshall, Paula L. Blanco, Miguel N. Burnier
Journal: Cancer Research (2005)

Proc Amer Assoc Cancer Res, Volume 46, 2005

6005 

Purpose: Cytokines are soluble secreted proteins that play a crucial role in angiogenesis, apoptosis, immune response and cell proliferation and differentiation. Several studies have shown that uveal melanoma (UM) cells express a large number of cytokines that are involved in tumor progression and are considered poor prognostic markers. The purpose of this study is to evaluate the simultaneous expression of various cytokines in the vitreous of an albino rabbit model of UM. Methods: Vitreous samples from an immunosuppressed rabbit model of UM were taken at the time of animal sacrifice throughout the twelve-week model. Ten vitreous samples were used in the cytokine assay (RayBiotech, Georgia, USA). The samples were diluted by 50% with 1x Blocking Buffer and the assays were run as per manufacturers specifications. The membranes were then exposed to Kodak x-omat AR film for 20 to 40 seconds to detect chemiluminescence. The relative intensity of the signal was subsequently rated. Results: Expression of six cytokines, including macrophage migration-inhibitory factor (MIF), tissue inhibitor of metalloproteinase-1 (TIMP-1), epidermal growth factor (EGF), vascular endothelial growth factor (VEGF), interferon-gamma (IFN- γ) and macrophage chemotactic protein-1 (MCP-1), was detected in the vitreous samples. Of the six cytokines detected, MIF, TIMP-1 and EGF were consistently highly expressed in all samples. Of the remaining cytokines, IFN-γ was detected in six samples, VEGF was detected in four samples, and MCP-1 was detected in one sample. Conclusions: Using an animal model of uveal melanoma, this study has identified the expression of various cytokines in the vitreous, an essential component within the ocular microenvironment, which may influence the progression of intra-ocular tumors. Further studies are warranted to investigate the role of these cytokines particularly MIF, TIMP-1 and EGF in UM progression.
P1.07-019 Large Cell Neuroendocrine Carcinoma of the Lung: Prognostic Factors of Survival and Recurrence after R0 Surgical Resection
Authors: Maria Cattoni, Eric Vallieres, Lisa Brown, Amir Sarkeshik, Stefano Margaritora, Alessandra Siciliani, Pier Luigi Filosso, Francesco Guerrera, Andrea Imperatori, Nicola Rotolo, Farhood Farjah, Grace Wandell, Kimberly Costas, Catherine Mann, Michal Hubka, Stephen Kaplan, Alexander Farivar, Ralph Aye, Brian Louie
Journal: Journal of Thoracic Oncology (2017)
Inflammatory Mediators in Mood Disorders: Therapeutic Opportunities
Authors: Madeline L. Pfau, Caroline Ménard, Scott J. Russo
Journal: The Annual Review of Pharmacology and Toxicology (2017)

Mood disorders such as depression are among the most prevalent psychiatric disorders in the United States, but they are inadequately treated in a substantial proportion of patients. Accordingly, neuropsychiatric research has pivoted from investigation of monoaminergic mechanisms to exploration of novel mediators, including the role of inflammatory processes. Subsets of mood disorder patients exhibit immune-related abnormalities, including elevated levels of proinflammatory cytokines, monocytes, and neutrophils in the peripheral circulation; dysregulation of neuroglia and blood-brain barrier function; and disruption of gut microbiota. The field of psychoneuroimmunology is one of great therapeutic opportunity, yielding experimental therapeutics for mood disorders, such as peripheral cytokine targeting antibodies, microglia and astrocyte targeting therapies, and probiotic treatments for gut dysbiosis, and producing findings that identify therapeutic targets for future development.
Ca2+ channel clustering with insulin-containing granules is disturbed in type 2 diabetes
Authors: Nikhil R. Gandasi, Peng Yin, Michela Riz, Margarita V. Chibalina, Giuliana Cortese, Per-Eric Lund, Victor Matveev, Patrik Rorsman, Arthur Sherman, Morten G. Pedersen, Sebastian Barg
Journal: Journal of Clinical Investigation (2017)

Loss of first-phase insulin secretion is an early sign of developing type 2 diabetes (T2D). Ca2+ entry through voltage-gated L-type Ca2+ channels triggers exocytosis of insulin-containing granules in pancreatic β cells and is required for the postprandial spike in insulin secretion. Using high-resolution microscopy, we have identified a subset of docked insulin granules in human β cells and rat-derived clonal insulin 1 (INS1) cells for which localized Ca2+ influx triggers exocytosis with high probability and minimal latency. This immediately releasable pool (IRP) of granules, identified both structurally and functionally, was absent in β cells from human T2D donors and in INS1 cells cultured in fatty acids that mimic the diabetic state. Upon arrival at the plasma membrane, IRP granules slowly associated with 15 to 20 L-type channels. We determined that recruitment depended on a direct interaction with the synaptic protein Munc13, because expression of the II-III loop of the channel, the C2 domain of Munc13-1, or of Munc13-1 with a mutated C2 domain all disrupted L-type channel clustering at granules and ablated fast exocytosis. Thus, rapid insulin secretion requires Munc13-mediated recruitment of L-type Ca2+ channels in close proximity to insulin granules. Loss of this organization underlies disturbed insulin secretion kinetics in T2D.
Immunotherapy Targets Several Different Pediatric Brain Tumors
Authors: Tracy Hampton
Journal: JAMA (2017)

Researchers have discovered that an antibody currently being evaluated in an early clinical trial against advanced adult non–central nervous system solid tumors effectively shrinks malignant masses in mouse models of different pediatric brain cancers.

The antibody, called Hu5F9-G4, blocks the CD47 protein, which is expressed on the surface of cells in many cancers and allows them to evade innate immune surveillance. Specifically, CD47 serves as an antiphagocytic or “don’t eat me” signal to macrophages by binding and activating an inhibitory protein expressed on the surface of myeloid cells.