tbuckley/cabot-search huggingface dataset:
Health-Related Tax Subsidies
Authors: William P. Brandon
Journal: New England Journal of Medicine (1982)

Politicians and policy analysts are increasingly questioning the wisdom of current health-related tax subsidies. Two administration task forces have recommended reductions in the tax incentives for the purchase of health insurance.1 , 2 In Congress several bills involving changes in health-related tax subsidies have been proposed (the Health Initiatives Reform Act of 1981, the Comprehensive Health-Care Reform Act, and the National Health-Care Reform Act of 1981).3 The Congressional Budget Office has produced several useful policy studies on tax expenditures generally and on tax expenditures related to the health sector, in particular.4 5 6 There are two reasons for the increased interest in health-related tax . . .
Cytologic Study of Gastric Aspirate for Carcinoma Cells&lt;xref ref-type="fn" rid="fn1"&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/xref&gt;&lt;xref ref-type="fn" rid="fn2"&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/xref&gt;
Authors: Henry C. Bryant, M. D., William R. Craig, M. D., H. Marvin Pollard, M. D.
Journal: JNCI Journal of the National Cancer Institute (1949)

Journal Article Cytologic Study of Gastric Aspirate for Carcinoma Cells Get access Henry C. Bryant, M. D., Henry C. Bryant, M. D. Search for other works by this author on: Oxford Academic PubMed Google Scholar William R. Craig, M. D., William R. Craig, M. D. Search for other works by this author on: Oxford Academic PubMed Google Scholar H. Marvin Pollard, M. D. H. Marvin Pollard, M. D. Department of Pathology and Department of Internal Medicine, University Hospital, University of Michigan Medical School, Ann Arbor, Mich. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 10, Issue 2, October 1949, Pages 459–466, https://doi.org/10.1093/jnci/10.2.459 Published: 01 October 1949
Issues with anti-Gr1 antibody-mediated myeloid-derived suppressor cell depletion
Authors: Yan-Fang Xing, Yu-Qi Zhou, Guo-Wei Ma, Ding-Yun Feng, Xiu-Rong Cai, Xing Li
Journal: Annals of the Rheumatic Diseases (2016)

Issues with anti-Gr1 antibody-mediated myeloid-derived suppressor cell depletionWe read with great interest the article 'Myeloid-derived suppressor cells have a proinflammatory role in the pathogenesis of autoimmune arthritis' by Chunqing Guo et al. 1 In this paper, the authors used anti-Gr1 antibody to deplete myeloid-derived suppressor cells (MDSCs) in arthritic mice and they found that it reduced disease severity and Th17 response.However, they did not report the efficiency of MDSC depletion.Anti-Gr1 antibody (RB6-8C5) was widely used and considered to be effective in eliminating MDSC.Srivastava et al 2 found that anti-Gr1 antibody led to a reduction in Gr1 + cells in tumour, blood, spleen and bone marrow (BM).Vincent Hurez used anti-Gr1 monoclonal antibody, which reduced MDSCs by 50%-75% in the spleen of tumour bearing (TB) mice, without reporting the results in BM and tumour. 3Zhang et al 4 found that anti-Gr1 antibody reduced MDSC by one-third in tumour.Thomas Condamine et al determined that anti-Gr1 antibody eliminated about 95% of MDSCs in spleen and blood of TB mice; however, it raised the immature myeloid cell (IMC) levels in the BM. 5 Ma et al 6 and Kumar et al 7 believed that anti-Gr1 antibody could not eliminate Ly6C high MDSCs.Besides, Ma et al 6 first indentified that anti-Gr1 antibody failed to reduce MDSCs in the liver.The liver might generate a more favourable environment for MDSCs. 5The present study did not present the efficacy of depletion at disease sites, spleen and BM.The efficacy of anti-Gr1 antibody was controversial.In the field of cancer, Srivastava et al, Zhang et al and many other researchers found that depletion of MDSCs by anti-Gr1 antibody led to the inhibition of tumour volume and tumour weight. 2 4 The results of Hurez et al 3 were different.Anti-Gr1-mediated depletion of MDSCs resulted in significantly slower tumour growth in the aged but not the young B16-bearing mice.The study by Kumar et al 7 did not find the anti-tumour efficacy of anti-Gr1 antibody.This inconsistence might influence other modes, such as arthritic mice in the present study.In summary, anti-Gr1 antibody (RB6-8C5) is widely used as an efficient agent for eliminating MDSCs in mice; however, its efficacy on each subtype of MDSCs, polymorphonuclear neutrophil MDSC (PMN-MDSC) and monocyte MDSC (M-MDSC) is still controversial.Meanwhile, there are more debates ongoing about its efficacy in disease control.Using novel methods to deplete MDSCs shall be an acceptable choice.
The Effect of Hypophysectomy and X Irradiation on Lymphoid Organs and on the Induction of Lymphoid Tumors in C57BL Mice&lt;xref ref-type="fn" rid="fn1"&gt;2&lt;/xref&gt;,&lt;xref ref-type="fn" rid="fn2"&gt;3&lt;/xref&gt;
Authors: Susan Nagareda, C., Kaplan, Henry S.
Journal: JNCI Journal of the National Cancer Institute (1955)

Journal Article The Effect of Hypophysectomy and X Irradiation on Lymphoid Organs and on the Induction of Lymphoid Tumors in C57BL Mice, Get access C. Susan Nagareda, C. Susan Nagareda Department of Radiology, Stanford University School of Medicine, San Francisco, Calif. Search for other works by this author on: Oxford Academic PubMed Google Scholar Henry S. Kaplan Henry S. Kaplan Department of Radiology, Stanford University School of Medicine, San Francisco, Calif. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 16, Issue 1, August 1955, Pages 139–152, https://doi.org/10.1093/jnci/16.1.139 Published: 01 August 1955 Article history Received: 24 January 1955 Published: 01 August 1955
Genome Therapy of Myotonic Dystrophy Type 1 iPS Cells for Development of Autologous Stem Cell Therapy
Authors: Yuanzheng Gao, Xiuming Guo, Katherine Santostefano, Yanlin Wang, Tammy Reid, Desmond Zeng, Naohiro Terada, Tetsuo Ashizawa, Guangbin Xia
Journal: Molecular Therapy (2016)

Myotonic dystrophy type 1 (DM1) is caused by expanded Cytosine-Thymine-Guanine (CTG) repeats in the 3'-untranslated region (3' UTR) of the Dystrophia myotonica protein kinase (DMPK) gene, for which there is no effective therapy. The objective of this study is to develop genome therapy in human DM1 induced pluripotent stem (iPS) cells to eliminate mutant transcripts and reverse the phenotypes for developing autologous stem cell therapy. The general approach involves targeted insertion of polyA signals (PASs) upstream of DMPK CTG repeats, which will lead to premature termination of transcription and elimination of toxic mutant transcripts. Insertion of PASs was mediated by homologous recombination triggered by site-specific transcription activator-like effector nuclease (TALEN)-induced double-strand break. We found genome-treated DM1 iPS cells continue to maintain pluripotency. The insertion of PASs led to elimination of mutant transcripts and complete disappearance of nuclear RNA foci and reversal of aberrant splicing in linear-differentiated neural stem cells, cardiomyocytes, and teratoma tissues. In conclusion, genome therapy by insertion of PASs upstream of the expanded DMPK CTG repeats prevented the production of toxic mutant transcripts and reversal of phenotypes in DM1 iPS cells and their progeny. These genetically-treated iPS cells will have broad clinical application in developing autologous stem cell therapy for DM1.
Chronic Graft-Versus-Host Disease after Allogeneic Stem Cell Transplant with in Vivo T-Cell Depletion By Alemtuzumab: Incidence, Outcome and Pattern of Organ Involvement
Authors: Maria Chiara Finazzi, Cristina Boschini, Janice Ward, Charles Craddock, Alessandro Rambaldi, Ram Malladi
Journal: Blood (2014)
P0574 : A signature of elevated immune activation is observed in the peripheral blood of virally suppressed, HBeAg-negative chronic HBV patients
Authors: C. Frey, A. Palazzo, L. Li, Menashe Elazar, E. Pham, B. Fram, T. Nguyen, H. Han, None Monica Elazar, J. Glenn, A. Ahmed, S. Pflanz
Journal: Journal of Hepatology (2015)
Personal View: Learning to live in a medical household
Authors: Kate Billings
Journal: BMJ (2004)

My two younger brothers and I have had a very medicine oriented upbringing. Our father is a surgeon with a special interest, and our mother is a general practitioner. Having reached the age of 21, I thought it would be interesting to reflect on how our childhoods have been affected by our parents' profession. My brothers and I have grown up with very different career aspirations to theirs.
Pharmacist Scope of Practice
Journal: Annals of Internal Medicine (2002)

This paper explores the increased scope of practice of U.S. pharmacists. It presents background information on the pharmacy profession and outlines how the medical profession can work with pharmacists to enhance patient safety and quality of care. The paper calls for further research on the effects of pharmacy automation and the move to the Doctor of Pharmacy degree on pharmacy practice. Other positions include support for patient education and hospital rounds, opposition to independent pharmacist prescriptive privileges and initiation of drug therapy, increased use of the pharmacist as immunizer (as allowed by state law), and continued support for the American College of Physicians–American Society of Internal Medicine 1990 therapeutic substitution position.
Is increased hepatitis C virus case‐finding combined with current or 8‐week to 12‐week direct‐acting antiviral therapy cost‐effective in UK prisons? A prevention benefit analysis
Authors: Natasha K. Martin, Peter Vickerman, Iain F. Brew, Joan Williamson, Alec Miners, William L. Irving, Sushma Saksena, Sharon J. Hutchinson, Sema Mandal, Eamonn O'Moore, Matthew Hickman
Journal: Hepatology (2016)

Prisoners have a high prevalence of hepatitis C virus (HCV), but case‐finding may not have been cost‐effective because treatment often exceeded average prison stay combined with a lack of continuity of care. We assessed the cost‐effectiveness of increased HCV case‐finding and treatment in UK prisons using short‐course therapies. A dynamic HCV transmission model assesses the cost‐effectiveness of doubling HCV case‐finding (achieved through introducing opt‐out HCV testing in UK pilot prisons) and increasing treatment in UK prisons compared to status quo voluntary risk‐based testing (6% prison entrants/year), using currently recommended therapies (8‐24 weeks) or interferon (IFN)‐free direct‐acting antivirals (DAAs; 8‐12 weeks, 95% sustained virological response, £3300/week). Costs (British pounds, £) and health utilities (quality‐adjusted life years) were used to calculate mean incremental cost‐effectiveness ratios (ICERs). We assumed 56% referral and 2.5%/25% of referred people who inject drugs (PWID)/ex‐PWID treated within 2 months of diagnosis in prison. PWID and ex‐PWID or non‐PWID are in prison an average 4 and 8 months, respectively. Doubling prison testing rates with existing treatments produces a mean ICER of £19,850/quality‐adjusted life years gained compared to current testing/treatment and is 45% likely to be cost‐effective under a £20,000 willingness‐to‐pay threshold. Switching to 8‐week to 12‐week IFN‐free DAAs in prisons could increase cost‐effectiveness (ICER £15,090/quality‐adjusted life years gained). Excluding prevention benefit decreases cost‐effectiveness. If &gt;10% referred PWID are treated in prison (2.5% base case), either treatment could be highly cost‐effective (ICER&lt;£13,000). HCV case‐finding and IFN‐free DAAs could be highly cost‐effective if DAA cost is 10% lower or with 8 weeks' duration. Conclusions: Increased HCV testing in UK prisons (such as through opt‐out testing) is borderline cost‐effective compared to status quo voluntary risk‐based testing under a £20,000 willingness to pay with current treatments but likely to be cost‐effective if short‐course IFN‐free DAAs are used and could be highly cost‐effective if PWID treatment rates were increased. (H epatology 2016;63:1796‐1808)
The Uptake of 18F-FDG by Renal Allograft in Kidney Transplant Recipients Is Not Influenced by Renal Function
Authors: Alexandre Jadoul, Pierre Lovinfosse, Laurent Weekers, Pierre Delanaye, Jean-Marie Krzesinski, Roland Hustinx, François Jouret
Journal: Clinical Nuclear Medicine (2016)

F-FDG PET/CT has been recently proposed as a noninvasive tool for the diagnosis of renal allograft acute rejection (AR) in kidney transplant recipients (KTRs). Still, the influence of kidney function on F-FDG uptake by renal grafts remains unknown.We retrospectively identified all KTRs who underwent at least one F-FDG PET/CT. Kidney transplant recipients with documented pyelonephritis or AR were excluded. Estimated glomerular filtration rate (eGFR) was assessed using chronic kidney disease (CKD)-EPI equation. Mean standardized uptake values (SUVmean) of renal graft cortex and aorta were measured in 4 and 1 volumes of interest, respectively. Spearman rank correlation coefficient (ρ) and analysis of variance (ANOVA) were performed.Eighty-two KTRs underwent F-FDG PET/CT for tumor staging (n = 46), suspected infection (n = 11), or fever of unknown origin (n = 25). Mean eGFR was 50 ± 19 mL/min per 1.73 m, including CKD stage 1 (n = 3), stage 2 (n = 21), stage 3a (n = 20), stage 3b (n = 29), and stage 4 (n = 9). Mean kidney and aorta SUVmean were 1.8 ± 0.2 and 1.7 ± 0.3, respectively. No significant correlation was observed between eGFR and kidney SUVmean (ρ, 0.119; P, 0.28) or aorta SUVmean (ρ, -0.144; P, 0.20). ANOVA showed no difference of kidney (P, 0.62) and aorta (P, 0.85) SUVmean between CKD groups. Mean coefficient of variation (on the basis of kidney SUVmean of >3 consecutive F-FDG PET/CT in 15 patients with no significant change of eGFR) reached 13.1%.The uptake of F-FDG by renal allografts within an hour postinjection is not significantly impacted by CKD.
ON THE BEHAVIOUR OF LEUCOCYTES IN MALIGNANT GROWTHS
Authors: J. B. Farmer, J. E. S. Moore, C. E. Walker
Journal: BMJ (1905)

LAu. I2, 19o5.may well imagine we have come into a vast cathedral from whose roof there echoes to us the sound of the voice of one of our brethren of the centuries B.C., of whom Addison tells us
Adipocyte‐specific overexpression of retinol‐binding protein 4 causes hepatic steatosis in mice
Authors: Seung‐Ah Lee, Jason J. Yuen, Hongfeng Jiang, Barbara B. Kahn, William S. Blaner
Journal: Hepatology (2016)

There is considerable evidence that both retinoids and retinol‐binding protein 4 (RBP4) contribute to the development of liver disease. To understand the basis for this, we generated and studied transgenic mice that express human RBP4 (hRBP4) specifically in adipocytes. When fed a chow diet, these mice show an elevation in adipose total RBP4 (mouse RBP4 + hRBP4) protein levels. However, no significant differences in plasma RBP4 or retinol levels or in hepatic or adipose retinoid (retinol, retinyl ester, and all‐ trans ‐retinoic acid) levels were observed. Strikingly, male adipocyte‐specific hRBP4 mice fed a standard chow diet display significantly elevated hepatic triglyceride levels at 3‐4 months of age compared to matched littermate controls. When mice were fed a high‐fat diet, this hepatic phenotype, as well as other metabolic phenotypes (obesity and glucose intolerance), worsened. Because adipocyte‐specific hRBP4 mice have increased tumor necrosis factor‐α and leptin expression and crown‐like structures in adipose tissue, our data are consistent with the notion that adipose tissue is experiencing RBP4‐induced inflammation that stimulates increased lipolysis within adipocytes. Our data further establish that elevated hepatic triglyceride levels result from increased hepatic uptake of adipose‐derived circulating free fatty acids. We obtained no evidence that elevated hepatic triglyceride levels arise from increased hepatic de novo lipogenesis, decreased hepatic free fatty acid oxidation, or decreased very‐low‐density lipoprotein secretion. Conclusion: Our investigations establish that RBP4 expressed in adipocytes induces hepatic steatosis arising from primary effects occurring in adipose tissue. (H epatology 2016;64:1534‐1546)
Abstract B2-04: Time lapse to cancer: Defining the transition from polyp to colorectal cancer based on telomere metrics
Authors: Brooke R. Druliner, Ruth Johnson, Xiaoyang Ruan, Russell Vanderboom, Donna Felmlee Devine, Jill Washechek Aletto, Lisa A. Boardman
Journal: Cancer Research (2015)

Abstract Despite advances in prevention and early detection strategies, colorectal cancer (CRC) remains the second leading cause of cancer death in the United States. The majority of CRC arises from adenomatous polyps. However, only 5% of all people who receive a colonoscopy will have a lesion determined to be at high risk for malignant transformation. Adenomas are primarily classified based on histology, size, degree of dysplasia and limited genetic mutation information. Further characterization of what contributes to or underlies the malignant transformation of polyps is currently lacking, but is essential to further understand the transition from polyp to cancer and factors that lead only a small portion of polyps to progress onto cancer. Although telomere length is a recognized biomarker in multiple cancers, few studies have addressed the comprehensive role of telomeres in CRC progression. Telomere shortening is a fundamental feature of dividing cells related to the age of the cell and is implicated in carcinogenesis. Telomere length is not solely determined by attrition resulting from cell division, but also through telomere maintenance mechanisms (TMM), which are often exploited in malignant cells. In this study, we will measure the telomere profile (consisting of telomere length and TMM) in normal colon epithelium, polyps and the adjacent tumor trios and normal colon epithelium and cancer-free polyp pairs. Our aim is to determine which telomere features distinguish cancer adjacent polyps from cancer free polyps. This is an innovative approach for identifying the definable telomere-related properties that distinguish polyps with malignant potential that remain benign from those that transform to cancer and progress to invasive lesions. Further characterization of the molecular profile of polyps undergoing the transition to cancer that differentiate cancer free polyps has the potential to be utilized in designing optimal treatment options for patients with polyps that carry the risk of CRC. Citation Format: Brooke R. Druliner, Ruth Johnson, Xiaoyang Ruan, Russell Vanderboom, Donna Felmlee Devine, Jill Washechek Aletto, Lisa A. Boardman. Time lapse to cancer: Defining the transition from polyp to colorectal cancer based on telomere metrics. [abstract]. In: Proceedings of the AACR Special Conference on Computational and Systems Biology of Cancer; Feb 8-11 2015; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2015;75(22 Suppl 2):Abstract nr B2-04.
Abstract P6-04-05: Genotype-phenotype classification of triple negative breast cancers (TNBC) in women of African descent using the PAM50 NanoString platform and genomic data
Authors: OA Olayiwola, TO Ogundiran, A Hardeman, TF Yoshimatsu, W Clayton, A Adeoye, A Ademola, MA Ajani, G Khramtsova, TA Grushko, D Huo, Y Zheng, J Parker, C Perou, OI Olopade
Journal: Cancer Research (2016)

Abstract Introduction: TNBC has the highest mortality rate amongst all other breast cancer types due to its complex tumor heterogeneity and lack of well-defined molecular targets. It is known that women of African descent are two to three times more likely to develop TNBC compared to women of European ancestry, yet wide-scale genomic studies of African and African American breast tumors are limited. To elucidate genotypes and molecular subtypes associated with the most aggressive forms of breast cancer, we used the PAM50 NanoString platform to reclassify Nigerian (NG), African American (AA) and Caucasian (CA) tumors previously annotated by Immunohistochemistry (IHC), and correlated our findings to their germline genotype data obtained using high-throughput technologies. Methods: RNAs were isolated from formalin-fixed, paraffin embedded (FFPE) tumor tissues using the High Pure Paraffin Kit (Roche) following manufacturer's protocol, and assayed on NanoString nCounter Analysis System using a custom Nano110 (PAM50 + claudin-low &amp; VEGF signatures) probe set. Intrinsic subtyping and gene-expression data were evaluated using R statistical software. All study samples were previously annotated and subtyped by the ER/PR/HER2 IHC classifier. Genotypes were obtained from next generation sequencing or Illumina Human2.5M BeadChip platform using germline DNA from more than 2000 breast cancer cases and 2000 controls were studied. Results: To date, Intrinsic molecular subtyping by Nano110 has been completed on 69 NG, 81 AA and 74 CA tumors. Concordance between IHC and PAM50 was 59%, which is adequate and comparable to previous studies. Basal-like subtype was overrepresented and accounted for nearly 30% of NG and AA cases, compared to 17% in CA cases. HER2-enriched subtype was overrepresented only in NG cases (9%). The proportion with Luminal A tumors were 44% NG, 56% AA and 68% CA, respectively. Conclusions: PAM50 NanoString assay is reliable and high-throughput for molecular subtyping breast cancer using RNA extracted from FFPE tumors. Ongoing work will correlate PAM50 intrinsic subtypes to genotype data. Citation Format: Olayiwola OA, Ogundiran TO, Hardeman A, Yoshimatsu TF, Clayton W, Adeoye A, Ademola A, Ajani MA, Khramtsova G, Grushko TA, Huo D, Zheng Y, Parker J, Perou C, Olopade OI. Genotype-phenotype classification of triple negative breast cancers (TNBC) in women of African descent using the PAM50 NanoString platform and genomic data. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P6-04-05.
Acute Lymphocytic Leukemia in Children
Authors: R J Aur
Journal: JAMA (1969)

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Cellular Expression of Lymphocyte Function-Associated Antigen-1 and Intercellular Adhesion Molecule-1 in Normal Kidney Structures and in Renal Cancer
Authors: R Minervini, V Panichi, L Viganò, R Felipetto, V Gattai, M Cecchi, L Fiorentini, R Palla
Journal: European Urology (1994)