tbuckley/cabot-search huggingface dataset:
The Effect of Funding Cuts on the Utilization of an Oral Pathology Diagnostic Service
Authors: Deepika Chugh, R John McComb, David Mock
Journal: International Journal of Oral Science (2009)

To examine what impact the loss of funding had on the utilization of the oral pathology service.Biopsy records were retrieved and examined in the two year period before and after the elimination of the subsidies in 2003.After the loss of funding, there was a 31% decrease in the number of specimens submitted from practitioners in private practice, with the greatest drop noted in submissions from endodontists.Despite the immediate decrease in the number of biopsies submitted after the introduction of fee-for-service, the number of specimens being submitted appears to be on the rise again, as practitioners appear to recognize the value of a specialized oral pathology diagnostic service.
Health Impact Assessment: A Tool to Help Policy Makers Understand Health Beyond Health Care
Authors: Brian L. Cole, Jonathan E. Fielding
Journal: Annual Review of Public Health (2006)

Health impact assessment (HIA)—a combination of methods to examine formally the potential health effects of a proposed policy, program, or project—has received considerable interest over the past decade internationally as a practical mechanism for collaborating with other sectors to address the environmental determinants of health and to achieve more effectively the goals of population health promotion. Demand for HIA in the United States seems to be growing. This review outlines the common principles and methodologies of HIA and compares different approaches to HIA. Lessons learned from the related field of environmental impact assessment and from experience with HIA in other countries are examined. Possible avenues for advancing both the field and the broader goals of population health promotion are outlined.
Successful treatment of alveolar proteinosis by inhaled GM-CSF and intravenous rituximab
Authors: Sebastian Fähndrich, Philipp Lepper, Sven Henschke, Robert Bals, Heinrike Wilkens
Journal: European Respiratory Journal (2014)

We report a case of successful treatment of alveolar proteinosis by a combination of inhaled GM-CSF and intravenous administration of rituximab, a monoclonal antibody directed against the B-lymphocyte antigen CD20. Pulmonary alveolar proteinosis is a chronic disorder of surfactant clearance from the alveoli due to an impaired phagocytosis of alveolar macrophages.  A 49-year-old woman referred with progressive shortness of breath. Typical computed tomography of the chest visualizes geographic ground-glass opacity combined with interlobular septal thickening (crazy paving). Pulmonary function test showed severe impairment of diffusion capacity and apparent respiratory insufficiency. Therapeutic whole-lung lavage was performed several times without clinical benefit. Because of the presence of anti-granulocyte macrophage colony-stimulating factor (GM-CSF) autoantibodies, a combination of inhaled granulocyte/macrophage-colony stimulating factor (GM-CSF 250 µg/day; every second week ), with 4 courses of intravenous infusions of rituximab (1,000 mg day 1 and 15) was given every 3 months within one year.  Twelve months after the initiation of the treatment, dyspnea improved from NYHA III to NYHA I; in parallel, the DLCO, CT scan and P(A-a)O2 and alveolar-arterial oxygen tension difference in room air improved dramatically. Lung function and X-rays also improved.  This case shows that the combination of inhaled GM-CSF and Rituximab could be a treatment for pulmonary alveolar proteinosis.
Multicenter Randomized Controlled Trial of Conventional Versus Laparoscopic Surgery for Colorectal Cancer Within an Enhanced Recovery Programme: EnROL
Authors: Robin H. Kennedy, E. Anne Francis, Rose Wharton, Jane M. Blazeby, Philip Quirke, Nicholas P. West, Susan J. Dutton
Journal: Journal of Clinical Oncology (2014)

Laparoscopic resection and a multimodal approach known as an enhanced recovery program (ERP) have been major changes in colorectal perioperative care that have improved clinical outcomes for colorectal cancer resection. EnROL (Enhanced Recovery Open Versus Laparoscopic) is a multicenter randomized controlled trial examining whether the benefits of laparoscopy still exist when open surgery is optimized within an ERP.
Abstract 4228: Identification of distinct mammary cancer stem cells with differential requirements for the autophagy regulator FIP200
Authors: Syn K. Yeo, Jian Wen, Song Chen, Jun-Lin Guan
Journal: Cancer Research (2015)

Abstract Cancer stem cells (CSCs) contribute to intratumoral heterogeneity and have been implicated in disease relapse and drug resistance. Added to this complexity is the idea that distinct CSC populations can coexist within a tumor and hence, the understanding of this diversity is imperative for effective therapeutic targeting. In this study, we show the co-existence of distinct breast CSC populations which can be identified by ALDH+ and CD29+CD61+ markers respectively using the MMTV-PyMT driven mouse model of breast cancer. While both of these populations exhibit enhanced tumor initiating potential in Nude mice relative to bulk tumor cells, the CD29+CD61+ population have increased invasive abilities and display higher expression of epithelial to mesenchymal (EMT) associated genes. As autophagy has been associated with the acquisition of breast CSC traits, we went on to address the requirement for autophagy in ALDH+ and CD29+CD61+ populations through the deletion of the autophagy regulator, FIP200 in MMTV-PyMT driven tumors. Interestingly, FIP200 deletion only reduces the percentage of CD29+CD61+ cells but does not affect the percentage of ALDH+ cells. However, the tumor initiating properties of both ALDH+ and CD29+CD61+ cells were impaired upon FIP200 deletion. The decrease in the number and CSC potential of CD29+CD61+ cells correlated with diminished TGF-beta signalling upon FIP200 deletion as indicated by decreased TGF-b2, TGF-b3 and phospho-SMAD2 levels. FIP200 deletion also reduced STAT3 activation and it remains to be addressed whether this is responsible for decreased CSC potential in ALDH+ cells. Altogether, our results demonstrate the presence of distinct CSCs in MMTV-PyMT tumors with potentially distinct requirements for divergent signaling pathways. Importantly, we also show that the autophagy regulator FIP200 plays a crucial role in governing the CSC properties of these distinct CSC populations and could represent a potential therapeutic target against breast CSCs. Citation Format: Syn K. Yeo, Jian Wen, Song Chen, Jun-Lin Guan. Identification of distinct mammary cancer stem cells with differential requirements for the autophagy regulator FIP200. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4228. doi:10.1158/1538-7445.AM2015-4228
Cognitive–Behavioral Therapy for Insomnia in Knee Osteoarthritis: A Randomized, Double‐Blind, Active Placebo–Controlled Clinical Trial
Authors: Michael T. Smith, Patrick H. Finan, Luis F. Buenaver, Mercedes Robinson, Uzma Haque, Angela Quain, Erin McInrue, Dingfen Han, Jeannie Leoutsakis, Jennifer A. Haythornthwaite
Journal: Arthritis & Rheumatology (2015)

Objective Insomnia is prevalent among patients with knee osteoarthritis (OA). Research indicates that sleep disruption may amplify clinical pain by altering central pain modulation, suggesting that treatment of insomnia may improve pain. The aims of this study were to evaluate the efficacy of cognitive–behavioral therapy for insomnia (CBT‐I) in patients with knee OA, to determine whether improvements in sleep predict reduced pain, and to determine whether alterations in pain modulation mediate improvements in clinical pain. Methods We conducted a randomized, double‐blind, active placebo–controlled clinical trial of CBT‐I in 100 patients with knee OA and insomnia (mean ± SD age 59.4 ± 9.5 years). Patients were randomized (1:1) to receive either 8 sessions of CBT‐I or behavioral desensitization (placebo). We conducted in‐home polysomnography (PSG), diary assessment, and sensory tests of pain modulation at baseline, posttreatment, 3 months, and 6 months. Results Intent‐to‐treat analyses demonstrated substantial improvement in sleep in both groups of patients. Patients in the CBT‐I group had significantly greater reductions in wake after sleep onset (WASO), as measured by patient diary and PSG. Patients in both groups reported significant and comparable reductions in pain over 6 months, with one‐third reporting a 30% reduction in pain severity. Baseline‐to‐posttreatment reductions in WASO as measured by diary and PSG predicted subsequent decreases in clinical pain. This effect was significantly greater for CBT‐I compared with behavioral desensitization. No significant changes in laboratory measures of pain modulation were observed. Conclusion Compared with active placebo, CBT‐I was efficacious in reducing sleep maintenance insomnia. CBT‐I decreased clinical pain, but not pain modulation, suggesting that it has the potential to augment pain management in knee OA. Future work is needed to identify the mechanisms by which improved sleep reduces clinical pain.
Uniform approach to risk classification and treatment assignment for children with acute lymphoblastic leukemia.
Authors: M Smith, D Arthur, B Camitta, A J Carroll, W Crist, P Gaynon, R Gelber, N Heerema, E L Korn, M Link, S Murphy, C H Pui, J Pullen, G Reamon, S E Sallan, H Sather, J Shuster, R Simon, M Trigg, D Tubergen, F Uckun, R Ungerleider
Journal: Journal of Clinical Oncology (1996)

PURPOSE To define more uniform criteria for risk-based treatment assignment for children with acute lymphoblastic leukemia (ALL), the Cancer Therapy Evaluation Program (CTEP) of the National Cancer Institute (NCI) sponsored a workshop in September 1993. Participants included representatives from the Childrens Cancer Group (CCG), Pediatric Oncology Group (POG), Dana-Farber Cancer Institute (DFCI), St Jude Children's Research Hospital (SJCRH), and the CTEP. METHODS Workshop participants presented and reviewed data from ALL clinical trials, using weighted averages to combine outcome data from different groups. RESULTS For patients with B-precursor (ie, non-T, non-B) ALL, the standard-risk category (4-year event-free survival [EFS] rate, approximately 80%) will include patients 1 to 9 years of age with a WBC count at diagnosis less than 50,000/microL. The remaining patients will be classified as having high-risk ALL (4-year EFS rate, approximately 65%). For patients with T-cell ALL, different treatment strategies have yielded different conclusions concerning the prognostic significance of T-cell immunophenotype. Therefore, some groups/institutions will classify patients with T-cell ALL as high risk, while others will assign risk for patients with T-cell ALL based on the uniform age/WBC count criteria. Workshop participants agreed that the risk category of a patient may be modified by prognostic factors in addition to age and WBC count criteria, and that a common set of prognostic factors should be uniformly obtained, including DNA index (DI), cytogenetics, early response to treatment (eg, day-14 bone marrow), immunophenotype, and CNS status. CONCLUSIONS The more uniform approach to risk-based treatment assignment and to collection of specific prognostic factors should increase the efficiency of future ALL clinical research.
A Concise Promoter Region of the Heart Fatty Acid–Binding Protein Gene Dictates Tissue-Appropriate Expression
Authors: Qinghua Qian, Lyn Kuo, Yie-Teh Yu, Jeffrey N. Rottman
Journal: Circulation Research (1999)

Abstract —The heart fatty acid–binding protein (HFABP) is a member of a family of binding proteins with distinct tissue distributions and diverse roles in fatty acid metabolism, trafficking, and signaling. Other members of this family have been shown to possess concise promoter regions that direct appropriate tissue-specific expression. The basis for the specific expression of the HFABP has not been previously evaluated, and the mechanisms governing expression of metabolic genes in the heart are not completely understood. We used transient and permanent transfections in ventricular myocytes, skeletal myocytes, and nonmyocytic cells to map regulatory elements in the HFABP promoter, and audited results in transgenic mice. Appropriate tissue-specific expression in cell culture and in transgenic mice was dictated by 1.2 kb of the 5′-flanking sequence of FABP3 , the HFABP gene. Comparison of orthologous murine and human genomic sequences demonstrated multiple regions of near-identity within this promoter region, including a CArG-like element close to the TATA box. Binding and transactivation studies demonstrated that this element can function as an atypical myocyte enhancer–binding factor 2 site. Interactions with adjacent sites are likely to be necessary for fully appropriate, tissue-specific, developmental and metabolic regulation.
Clinical and pharmacokinetic phase II study of pegylated liposomal doxorubicin and vinorelbine in heavily pretreated recurrent ovarian carcinoma
Authors: D. Katsaros, M.V. Oletti, I.A. Rigault de la Longrais, A. Ferrero, A. Celano, S. Fracchioli, M. Donadio, R. Passera, L. Cattel, C. Bumma
Journal: Annals of Oncology (2005)
Inferring Selection on Amino Acid Preference in Protein Domains
Authors: A. M. Moses, R. Durbin
Journal: Molecular Biology and Evolution (2008)

Models that explicitly account for the effect of selection on new mutations have been proposed to account for "codon bias" or the excess of "preferred" codons that results from selection for translational efficiency and/or accuracy. In principle, such models can be applied to any mutation that results in a preferred allele, but in most cases, the fitness effect of a specific mutation cannot be predicted. Here we show that it is possible to assign preferred and unpreferred states to amino acid changing mutations that occur in protein domains. We propose that mutations that lead to more common amino acids (at a given position in a domain) can be considered "preferred alleles" just as are synonymous mutations leading to codons for more abundant tRNAs. We use genome-scale polymorphism data to show that alleles for preferred amino acids in protein domains occur at higher frequencies in the population, as has been shown for preferred codons. We show that this effect is quantitative, such that there is a correlation between the shift in frequency of preferred alleles and the predicted fitness effect. As expected, we also observe a reduction in the numbers of polymorphisms and substitutions at more important positions in domains, consistent with stronger selection at those positions. We examine the derived allele frequency distribution and polymorphism to divergence ratios of preferred and unpreferred differences and find evidence for both negative and positive selections acting to maintain protein domains in the human population. Finally, we analyze a model for selection on amino acid preferences in protein domains and find that it is consistent with the quantitative effects that we observe.
Understanding how combinations of HLA and KIR genes influence disease
Authors: Sumati Rajagopalan, Eric O. Long
Journal: The Journal of Experimental Medicine (2005)

Combinations of HLA and killer cell immunoglobulin-like receptor (KIR) genes have been associated with diseases as diverse as autoimmunity, viral infections, reproductive failure, and now cancer. Much as early observations of disease associations with HLA polymorphism preceded a detailed knowledge of HLA recognition by T cell receptors, the recently reported disease associations with HLA-KIR gene combinations beg for a better understanding of the underlying mechanisms.
Hepcidin and its role in iron absorption
Authors: K J Robson
Journal: Gut (2004)

Maintaining the correct iron balance is crucial to good health. Disorders of iron homeostasis have a global distribution. As iron is not actively excreted by the body, understanding the role of proteins involved in regulating iron uptake is essential to our understanding of disease involving iron homeostasis. Over the past 10 years, major advances have been made in understanding the genetics of iron metabolism and this has led to identification of a number of new proteins, including hepcidin, involved in iron homeostasis.
Epidemiology of <i>Pseudomonas aeruginosa</i> in Cystic Fibrosis in British Columbia, Canada
Authors: David P. Speert, Maureen E. Campbell, Deborah A. Henry, Ruth Milner, Fatma Taha, Anna Gravelle, A. George F. Davidson, Lawrence T. K. Wong, Eshwar Mahenthiralingam
Journal: American Journal of Respiratory and Critical Care Medicine (2002)

Pseudomonas aeruginosa is the most common respiratory pathogen in patients with cystic fibrosis (CF), but the predominant mechanism by which it is acquired is controversial. To determine the frequency of patient-to-patient spread, we evaluated P. aeruginosa isolates from 174 patients treated at the CF clinics in Vancouver, BC, Canada, since 1981. Multiple isolates were obtained from each patient and genetically typed by random amplified polymorphic DNA and pulsed field gel electrophoresis analyses. A total of 157 genetic types of P. aeruginosa was identified, 123 of which were unique to individual patients. A total of 34 types was shared by more than one patient; epidemiologic evidence linked these individuals only in the cases of 10 sibships and 1 pair of unrelated patients. We conclude that there is an extremely low risk in Vancouver for patients with CF to acquire P. aeruginosa from other patients. It appears that prolonged close contact, such as occurs between siblings, is necessary for patient-to-patient spread. The major source of acquisition of P. aeruginosa in CF appears to be from the environment. Considering these observations, we do not recommend segregation of patients with CF on the basis of their colonization status with P. aeruginosa.
AS03-adjuvanted versus non-adjuvanted inactivated trivalent influenza vaccine against seasonal influenza in elderly people: a phase 3 randomised trial
Authors: Janet E McElhaney, Jiri Beran, Jeanne-Marie Devaster, Meral Esen, Odile Launay, Geert Leroux-Roels, Guillermo M Ruiz-Palacios, Gerrit A van Essen, Adrian Caplanusi, Carine Claeys, Christelle Durand, Xavier Duval, Mohamed El Idrissi, Ann R Falsey, Gregory Feldman, Sharon E Frey, Florence Galtier, Shinn-Jang Hwang, Bruce L Innis, Martina Kovac, Peter Kremsner, Shelly McNeil, Andrzej Nowakowski, Jan Hendrik Richardus, Andrew Trofa, Lidia Oostvogels
Journal: The Lancet Infectious Diseases (2013)
Antibodies against human 60 kDa heat shock protein are not associated with cardiovascular disease in patients with rheumatoid arthritis
Authors: V P van Halm
Journal: Annals of the Rheumatic Diseases (2005)

Rheumatoid arthritis is associated with an unexplained increased risk of cardiovascular disease (CVD). Antibodies against human 60 kDa heat shock protein (anti-HSP60) are associated with the presence and severity of CVD.To investigate whether anti-HSP60 antibodies are associated with prevalent CVD in patients with rheumatoid arthritis.In a nested case-control design, anti-HSP60 antibody levels were measured in the serum samples of 192 rheumatoid patients. In a regression analysis the association between prevalent CVD and anti-HSP60 antibodies was examined, along with the possible influence on this association of several demographic, rheumatoid arthritis, and CVD related variables.In a random sample of 326 patients with rheumatoid arthritis, 48 cases were identified who also suffered from CVD. Three controls per case with rheumatoid arthritis but without CVD (n = 144) were matched for sex, age, disease duration, and smoking habits. A regression analysis showed no significant association between prevalent CVD and anti-HSP60 antibodies (odds ratio = 1.00 (95% confidence interval, 0.997 to 1.004)). After correcting for possible confounding variables, still no association was found.In contrast to the general population, anti-HSP60 antibody titres are not associated with prevalent CVD in patients with rheumatoid arthritis. These findings could be the result of an altered immune response to HSP60 in rheumatoid arthritis.
Novel mutation in the<i>CLDN1</i>gene in a Turkish family with neonatal ichthyosis sclerosing cholangitis (NISCH) syndrome
Authors: P. Kirchmeier, E. Sayar, A. Hotz, I. Hausser, A. Islek, A. Yilmaz, R. Artan, J. Fischer
Journal: British Journal of Dermatology (2013)

P.K. and E.S. contributed equally to this work. Funding sources: This study was supported by the Institute of Human Genetics at the University Medical Center Freiburg. I.H. was supported by a BMBF grant NIRK 016GM0904 The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Conflicts of interest: No conflicts of interest to disclose. Dear Editor, Neonatal ichthyosis sclerosing cholangitis (NISCH) syndrome (MIM #607626) also known as ichthyosis–hypotrichosis–sclerosing cholangitis (IHSC)1 is a rare autosomal recessive disorder characterized by scalp hypotrichosis, scarring alopecia, ichthyosis and sclerosing cholangitis. Additional clinical features include hair and teeth anomalies and in individual cases, mental retardation and bilateral uveal synechiae.2 3 NISCH syndrome is caused by mutations in the CLDN1 gene (MIM *603718) that encodes the tight junction protein claudin‐1.4 A lack of claudin‐1 leads to increased paracellular permeability between epithelial cells.4 5 Only two homozygous mutations (c.200delTT and c.358delG)3 4 in the CLDN1 gene have been reported in 12 patients from five families with NISCH syndrome to date.6 Here we describe two patients from a consanguineous family of Turkish origin with the clinical characteristics of NISCH syndrome who harbour a novel homozygous nonsense mutation in the CLDN1 gene (c.181C>T, p.Gln61X), which leads to a truncated protein.
Recurrent megajejunum in an adult
Authors: F Di Franco, O A Adedeji, J S Varma
Journal: Journal of the Royal Society of Medicine (2002)

Jejunoileal atresia is usually treated by excision, including the dilated proximal bowel, and primary anastomosis1. Morbidity is high during infancy1,2,3 but there are few reports of continued morbidity into teenage and adult life4,5,6.
Integrating bevacizumab, everolimus, and lapatinib into current neoadjuvant chemotherapy regimen for primary breast cancer. Safety results of the GeparQuinto trial
Authors: G. von Minckwitz, H. Eidtmann, S. Loibl, J.-U. Blohmer, S.-D. Costa, P.A. Fasching, R. Kreienberg, J. Hilfrich, B. Gerber, C. Hanusch, T. Fehm, D. Strumberg, C. Solbach, V. Nekljudova, M. Untch
Journal: Annals of Oncology (2010)
Why Do We Still Use Hormone Replacement Therapy? Why Don’t We Use It More?
Authors: Victor G. Vogel
Journal: Journal of Clinical Oncology (2002)

Article Tools EDITORIALS Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.2002.20.3.616 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 11821438 Why Do We Still Use Hormone Replacement Therapy? Why Don’t We Use It More? Victor G. VogelxVictor G. VogelSearch for articles by this author Show More University of Pittsburgh Cancer Institute, Magee-Womens Hospital, Pittsburgh, PA https://doi.org/10.1200/JCO.2002.20.3.616 First Page Full Text PDF Figures and Tables © 2002 by American Society of Clinical Oncology