tbuckley/cabot-search huggingface dataset:
The Physician's Responsibility toward Hopelessly Ill Patients
Authors: Sidney H. Wanzer, Daniel D. Federman, S. James Adelstein, Christine K. Cassel, Edwin H. Cassem, Ronald E. Cranford, Edward W. Hook, Bernard Lo, Charles G. Moertel, Peter Safar, Alan Stone, Jan van Eys
Journal: New England Journal of Medicine (1989)

Abstract Physicians have a specific responsibility toward patients who are hopelessly ill, dying, or in the end stages of an incurable disease. In a summary of current practices affecting the care of dying patients, we give particular emphasis to changes that have become commonplace since the early 1980s. Implementation of accepted policies has been deficient in certain areas, including the initiation of timely discussions with patients about dying, the solicitation and execution in advance of their directives for terminal care, the education of medical students and residents, and the formulation of institutional guidelines. The appropriate and, if necessary, aggressive use of pain-relieving substances is recommended, even when such use may result in shortened life. We emphasize the value of a sensitive approach to care — one that is adjusted continually to suit the changing needs of the patient as death approaches. Possible settings for death are reviewed, including the home, the hospital, the intensive care unit, and the nursing home. Finally, we consider the physician's response to the dying patient who is rational and desires suicide or euthanasia. (N Engl J Med 1989; 320:844–9.)
Purification and IgE-binding properties of peanut allergen Ara h 6*1Evidence for cross-reactivity with Ara h2
Authors: S.J. Koppelman, G.A.H. de Jong, M. Ertmann, M. Wensing, S.L. Hefle, A.C. Knulst, E.F. Knol
Journal: Journal of Allergy and Clinical Immunology (2004)
Abstract 4025: Combination strategy of endoscopic resection and telomerase-targeting oncolytic virus for eradicating lymph node metastasis of submucosal invasive colorectal cancer
Authors: Naoto Hori, Satoru Kikuchi, Hiroyuki Kishimoto, Hiroshi Tazawa, Yuuri Hashimoto, Shinji Kuroda, Shunsuke Kagawa, Yasuo Urata, Robert M. Hoffman, Toshiyoshi Fujiwara
Journal: Cancer Research (2014)

Abstract Endoscopic resection is now one of the options as minimally invasive therapy for early colorectal cancer, However, surgical resection has been still standard for submucosal invasive colorectal cancer, because about 10% of that have LN metastasis. To secure endoscopic resection for submucosal invasive colorectal cancer, an alternative, innovational strategy to purge potential LN metastasis is required. We previously reported that a telomerase-dependent oncolytic adenovirus (OBP-301) spreads to the regional LNs, selectively replicates, and eradicates metastatic cancer cells in LNs, when administered into the orthotopically xenotransplanted rectal tumor in mouse model. In this study we evaluated whether OBP-301 could inhibit LN metastasis after the local resection mimicking endoscopic resection in a submucosal invasive rectal tumor mouse model. Human colon cancer HCT-116 cells expressing green fluorescent protein (GFP) were orthotopically implanted into the submucosal layer of the rectum in nude mouse, to develop resultant rectal tumor mimicking submucosal invasive one. LN metastasis was observed in 78.5% of mice as early as 7 days after cancer cell inoculation. The rectal tumor was injected with OBP-301 peritumorally, and then got locally excised mimicking Endoscopic submucosal dissection (ESD) technique. Seven days after tumor resection, the treatment with OBP-301 showed a significant inhibition in LN metastasis, whereas the other control treatment did not. Moreover, LN metastatic recurrence was not detected in OBP-301-treated group even 4 weeks after tumor resection. Similar results were also observed in another model with human colon cancer Colo-205-GFP cells. These results suggest that a novel combination of ESD and OBP-301 might have potential to take place of the conventional surgical approach in treating submucosal invasive colorectal cancer. Citation Format: Naoto Hori, Satoru Kikuchi, Hiroyuki Kishimoto, Hiroshi Tazawa, Yuuri Hashimoto, Shinji Kuroda, Shunsuke Kagawa, Yasuo Urata, Robert M. Hoffman, Toshiyoshi Fujiwara. Combination strategy of endoscopic resection and telomerase-targeting oncolytic virus for eradicating lymph node metastasis of submucosal invasive colorectal cancer. [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 4025. doi:10.1158/1538-7445.AM2014-4025
Multigenic investigation of sequence variants in DNA repair and cell cycle control pathways on risk of lung cancer
Authors: Rayjean J. Hung, Paul Brennan, Federico Canzian, Janet Hall, Paolo Boffetta
Journal: Cancer Research (2005)

Proc Amer Assoc Cancer Res, Volume 46, 2005

2559 

Background . Genetic association studies on lung cancer aim to identify common low-risk susceptibility genes, however, most of such studies are underpowered and limited to single marker analysis. As lung cancer susceptibility is likely to have a polygenic basis, we have conducted a large multicenter case-control study to investigate multiple sequence variants in DNA repair and cell cycle control pathways that are essential for genome integrity and replication accuracy. Methods . A total of 2633 lung cancer cases and 2884 controls were recruited in Czech Republic, Hungary, Poland, Romania, Russia and Slovakia. Subjects completed a detailed lifestyle questionnaire and provided a blood sample. Initial results on 12 sequence variants in 8 candidate genes were available for 2092 cases and 1433 controls (MGMT C171T, Ile143Val, Lys178Arg; XPF Pro379Ser, Arg415Gln; XRCC2 Arg188His, XRCC3 Thr241Met, CCND1 G870A, CDKN2A Ala148Thr, TP53 Arg72Pro and a 16 bp repeat in TP53 intron3). We applied E-M algorithm to estimate the haplotype frequency for the multiple variants in MGMT, XPF, and TP53. Effect modifications of age of onset and smoking were evaluated. Combining with previously reported data on 6 additional polymorphisms in DNA repair pathway (OGG1 Ser326Cys, XRCC1 Arg194Trp, Arg280His, Arg399Gln, APEX Gln51His and XPD Lys751Gln), we conducted multigenic analyses on a total of 18 potential low-penetrance sequence variants. Cases with family history (as who had at least one first degree relative with lung cancer) were analyzed separately. Results . The results of MGMT haplotype analysis suggested that the haplotype of 171T-143Val-178Arg increased risk of lung cancer with OR of 1.24 (95%CI=1.02-1.50). XRCC3 Met/Met genotype conferred a protective effect overall (OR=0.75, 95%CI=0.59-0.95), and among cases with family history (OR=0.54, 95%CI=0.3-1.00). A 16 bp repeat in TP53 intron 3 and Arg72Pro was shown to be in linkage disequilibrium (D’=0.82), however, an increased risk of lung cancer was mainly observed in carriers of TP53 intron 3 homozygous variants (OR=1.93, 95%CI=1.26-2.96 overall, OR=2.65, 95%CI=1.16-6.09 for cases with family history). Multigenic analysis of the 18 polymorphisms suggested an increased risk with OR of 2.01 (95%CI=1.20-3.37) when the subjects carried at least 8 prior risk genotypes (Trend P =0.006). When the multigenic analysis was restricted to the 6 variants that showed a main effect in our study population under a multiplicative model, every increment in the number of prior risk genotypes conferred ORs of 1.30 (95%CI=1.17-1.44) overall and 1.26 (95%CI=0.99-1.61) among cases with family history. Conclusions . In summary, although common genetic polymorphisms may not individually confer a detectable increased risk of lung cancer, analyzing multiple alleles simultaneously may provide a more complete picture of cancer susceptibility.
WEIGHT REDUCTION IN AN OBESE DIABETIC
Authors: J R KINNEY
Journal: Annals of Internal Medicine (1954)

Case Reports1 May 1954WEIGHT REDUCTION IN AN OBESE DIABETICJANET R. KINNEY, M.D.JANET R. KINNEY, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-40-5-1024 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe relationship of metabolic and psychogenic factors in diabetes is illustrated graphically by the following case history.CASE REPORTA 46 year old white female was seen in the diabetic clinic of St. Luke's Hospital on December 31, 1943, as a problem in diabetic management. She had noted the onset of polyuria, polydipsia and dryness of the mouth in 1941. In two years of clinic management her weight and insulin requirements had steadily risen. She now weighed over 300 pounds, and her insulin dosage was 90 units protamine zinc insulin and 90 units of regular insulin. The blood sugar was...Bibliography1. Dunbar F: Psychosomatic diagnosis, 1943, Hoeber, New York, pp. 481-541. Google Scholar2. Joslin EP: Treatment of diabetes mellitus, 1946, Lea & Febiger, Philadelphia, pp. 68-80. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Chicago, Illinois*Received for publication August 24, 1953.From the Department of Medicine, University of Illinois. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byRemission in Diabetes 1 May 1954Volume 40, Issue 5Page: 1024-1026KeywordsBlood sugarInsulinMouthOverweightProtaminesWeight lossZinc ePublished: 1 December 2008 Issue Published: 1 May 1954 PDF downloadLoading ...
Slow Card Uptake
Authors: Brian Vastag
Journal: JAMA (2004)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Abstract 11923: FLNC Gene Splice Mutation Causes Dilated Cardiomyopathy in Two Families
Authors: Rene L Begay, August Martin, Sharon L Graw, Dobromir B Slavov, Charles A Tharp, Mary Sweet, Francesca Brun, Kenneth L Jones, Katherine Gowan, Daniela Miani, Gianfranco Sinagra, Luisa Mestroni, Deborah M Garrity, Matthew R Taylor
Journal: Circulation (2014)

Background: Dilated cardiomyopathy (DCM) is an important and frequently genetic cause of heart failure. Over 30 DCM genes have been described, the majority of which encode proteins that contribute to cytoskeletal and sarcomeric structures. Only 30-40% of cases can be attributed to a known DCM gene, motivating the ongoing search for novel disease genes. Methods and Results: We performed whole exome sequencing (WES) in a multigenerational DCM family from Northern Italy in whom prior DCM genetic testing had been unrevealing. Pathogenic variants were sought by a combination of bioinformatic filtering and cosegregation among affected individuals within the family. Thirteen gene candidates were identified including one novel variant in FLNC (filamin-C gene), already linked to a skeletal muscle disease phenotype. We further noted that WES found the identical variant in a second smaller family from the same geographical area; the mutation was present on a common haplotype. The variant is located in the 3’ end of ...
Abstract 17423: Unique Features of Cortical Bone Stem Cells Associated With Enhanced Cardiac Repair
Authors: Sadia Mohsin, Thomas E Sharp, Shavonn Smith, Hajime Kubo, Remus M Berretta, Joshua M Hare, Steven R Houser
Journal: Circulation (2014)

Rationale: Adoptive transfer of bone marrow and cardiac derived stem cells (CDCs) into failing human hearts has been shown to be safe, yet these cells have induced modest improvements in myocardial function. Recently we have shown in a mouse model that cortical bone derived stem cells (CBSCs) induced a greater enhancement of cardiac function after myocardial infarction than CDCs, possibly through enhanced paracrine signaling and transdifferentiation of the transplanted cells. However, the relative reparative potential of CBSCs relative to other known stem cell types including bone marrow derived mesenchymal stem cells (MSCs) and cardiac derived stem cells (CDCs) is not known. Objective: To characterize surface marker expression, proliferation, survival and differentiation capacity of swine CBSCs relative to MSCs and CDCs. Methods and Results: CBSCs, MSCs and CDCs were isolated from cortical bone, bone marrow and heart (left ventricle) of Gottingen miniswine. CBSCs were morphologically distinct from MSCs a...
Diagnosis of chronic disseminated candidosis from liver biopsies by a novel PCR in patients with haematological malignancies
Authors: M. Fleischhacker, S. Schulz, K. Jöhrens, M. von Lilienfeld-Toal, T. Held, E. Fietze, C. Schewe, I. Petersen, M. Ruhnke
Journal: Clinical Microbiology and Infection (2011)
Expression of CD26/dipeptidyl-peptidase IV in benign and malignant pigment-cell lesions of the skin
Authors: None Van Den Oord
Journal: British Journal of Dermatology (1998)

The T-cell activation antigen CD26 or dipeptidyl-peptidase IV (DPP-IV) belongs to a group of membrane-bound proteases that are variably expressed by melanoma cell lines. In vitro studies have suggested that loss of CD26 is associated with tumour progression. To correlate its expression with the histological stage of tumour progression of malignant melanoma (MM), we studied the distribution of CD26/DPP-IV in paraffin sections of a series of 110 benign and malignant pigment-cell lesions of the skin using a cocktail of anti-CD26 monoclonal antibodies and the three-step ABC method. Only two of 44 benign lesions focally expressed CD26 in their junctional compartment. In MM, expression of CD26 was not related to any of the known histological prognostic factors, but was associated with the stage of tumour progression; thus, CD26 was expressed in the situ or invasive radial growth phase in 34% of MM, whereas only 12% of MM expressed CD26 in the vertical growth phase. No CD26 expression occurred in metastatic melanomas. These data suggest that this proteinase plays a part in the early invasion of MM. Thus, CD26 may serve in the binding to, and enzymatic degradation, components of the extracellular matrix of the papillary dermis. Loss of CD26 in the vertical growth phase may contribute to the insufficient inactivation of regulatory peptides and unlimited action of growth factors.
Mechanisms of PD-L1/PD-1–mediated CD8 T-cell dysfunction in the context of aging-related immune defects in the Eµ-TCL1 CLL mouse model
Authors: Fabienne McClanahan, John C. Riches, Shaun Miller, William P. Day, Eleni Kotsiou, Donna Neuberg, Carlo M. Croce, Melania Capasso, John G. Gribben
Journal: Blood (2015)
Abstract 115: SMYD2-mediated methylation regulates PTEN activity
Authors: Makoto Nakakido, Yusuke Nakamura, Ryuji Hamamoto
Journal: Cancer Research (2015)

Abstract PTEN is a well characterized tumor suppressor protein. PTEN counteract PI3K-AKT pathway, which is one of the key signaling pathway for human tumorigenesis, through its lipid phosphatase activity. Whereas PTEN is known to be modified with various kinds of post-translational modifications such as phosphorylation, acetylation, and ubiquitination, methylation has not been reported to date. In this study, we elucidated SMYD2 (SET and MYND domain containing 2), a protein methyltransferase related to human tumorigenesis, methylated PTEN at lysine 313 in C2 domain. SMYD2 knockdown caused downregulation of PI3K-AKT pathway and led to cell growth suppression, suggesting that SMYD2-mediated PTEN methylation would negatively regulate PTEN activity. Given the critical role of PTEN as a tumor suppressor, our finding would not only contribute to further understanding of the mechanism of SMYD2 depending human tumorigenesis, but also may lead to a novel anti-cancer therapeutic strategy. Citation Format: Makoto Nakakido, Yusuke Nakamura, Ryuji Hamamoto. SMYD2-mediated methylation regulates PTEN activity. [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 115. doi:10.1158/1538-7445.AM2015-115
Ovarian cancer and smoking: individual participant meta-analysis including 28 114 women with ovarian cancer from 51 epidemiological studies
Authors: E. E. Calle, S. M. Gapstur, A. V. Patel, L. Dal Maso, R. Talamini, A. Chetrit, G. Hirsh-Yechezkel, F. Lubin, Siegal Sadetzki, E. Banks, V. Beral, D. Bull, K. Callaghan, B. Crossley, K. Gaitskell, A. Goodill, J. Green, C. Hermon, T. Key, K. Moser, G. Reeves, F. Sitas, R. Collins, R. Doll, R. Peto, C. A. Gonzalez, N. Lee, P. Marchbanks, H. W. Ory, H. B. Peterson, P. A. Wingo, N. Martin, T. Pardthaisong, S. Silpisornkosol, C. Theetranont, B. Boosiri, S. Chutivongse, P. Jimakorn, P. Virutamasen, C. Wongsrichanalai, A. Tjonneland, L. Titus-Ernstoff, T. Byers, T. Rohan, B. J. Mosgaard, M. Vessey, D. Yeates, J. L. Freudenheim, J. Chang-Claude, Rudolf Kaaks, K. E. Anderson, A. Folsom, K. Robien, J. Hampton, P. A. Newcomb, M. A. Rossing, D. B. Thomas, N. S. Weiss, E. Riboli, F. Clavel-Chapelon, D. Cramer, S. E. Hankinson, S. S. Tworoger, S. Franceschi, C. La Vecchia, E. Negri, H. O. Adami, C. Magnusson, T. Riman, Elisabete Vainio Weiderpass, A. Wolk, L. J. Schouten, P. A. van den Brandt, N. Chantarakul, S. Koetsawang, D. Rachawat, D. Palli, A. Black, L. A. Brinton, D. M. Freedman, P. Hartge, A. W. Hsing, Jr V. Lacey, R. N. Hoover, C. Schairer, M. Urban, S. Graff-Iversen, R. Selmer, C. J. Bain, A. C. Green, D. M. Purdie, V. Siskind, P. M. Webb, K. Moysich, S. E. McCann, P. Hannaford, C. Kay, C. W. Binns, A. H. Lee, M. Zhang, R. B. Ness, P. Nasca, P. F. Coogan, J. R. Palmer, L. Rosenberg, J. Kelsey, R. Paffenbarger, A. Whittemore, K. Katsouyanni, A. Trichopoulou, D. Trichopoulos, A. Tzonou, A. Dabancens, L. Martinez, R. Molina, O. Salas, M. T. Goodman, G. Lurie, M. E. Carney, L. R. Wilkens, L. Hartman, J. Manjer, H. Olsson, J. A. Grisso, M. Morgan, J. E. Wheeler, C. H. Bunker, R. P. Edwards, F. Modugno, P. H M Peeters, J. Casagrande, M. C. Pike, R. K. Ross, A. H. Wu, A. B. Miller, M. Kumle, I. T. Gram, E. Lund, L. McGowan, X. O. Shu, W. Zheng, T. M M Farley, S. Holck, O. Meirik, H. A. Risch
Journal: The Lancet Oncology (2012)
Vinblastine fails to improve response of renal cancer to interferon alfa-n1: high response rate in patients with pulmonary metastases.
Authors: J A Neidhart, S A Anderson, J E Harris, J J Rinehart, J Laszlo, F H Dexeus, L H Einhorn, D L Trump, P W Benedetto, R L Tuttle
Journal: Journal of Clinical Oncology (1991)

One hundred sixty-five patients were randomized to receive either interferon alfa-n1 (Wellferon; Burroughs Wellcome Co, Research Triangle Park, NC) alone or with vinblastine. An initial six-cycle induction treatment consisted of interferon given at daily doses of 3, 5, 20, 20, and 20 x 10(6) U/m2 every 2 weeks. Vinblastine at a dose of 10 mg/m2 (later decreased to 5 mg/m2) was given on day 1 of alternate cycles. Toxicities were generally well tolerated. The overall response rate was 10% with no significant difference between treatment arms. Survival was also not significantly different for the arms. A small subset of patients (16) with metastases only to the lungs had a high complete response (CR) and partial response (PR) rate of 44%. Responses were durable, and overall survival of this group was much better than that of the other patients.
Allergen cross reactions: a problem greater than ever thought?
Authors: P. Pfiffner, R. Truffer, P. Matsson, C. Rasi, A. Mari, B. M. Stadler
Journal: Allergy (2010)

Cross reactions are an often observed phenomenon in patients with allergy. Sensitization against some allergens may cause reactions against other seemingly unrelated allergens. Today, cross reactions are being investigated on a per-case basis, analyzing blood serum specific IgE (sIgE) levels and clinical features of patients suffering from cross reactions. In this study, we evaluated the level of sIgE compared to patients' total IgE assuming epitope specificity is a consequence of sequence similarity.Our objective was to evaluate our recently published model of molecular sequence similarities underlying cross reactivity using serum-derived data from IgE determinations of standard laboratory tests. We calculated the probabilities of protein cross reactivity based on conserved sequence motifs and compared these in silico predictions to a database consisting of 5362 sera with sIgE determinations.Cumulating sIgE values of a patient resulted in a median of 25-30% total IgE. Comparing motif cross reactivity predictions to sIgE levels showed that on average three times fewer motifs than extracts were recognized in a given serum (correlation coefficient: 0.967). Extracts belonging to the same motif group co-reacted in a high percentage of sera (up to 80% for some motifs).Cumulated sIgE levels are exaggerated because of a high level of observed cross reactions. Thus, not only bioinformatic prediction of allergenic motifs, but also serological routine testing of allergic patients implies that the immune system may recognize only a small number of allergenic structures.
Commentary: are methotrexate and azathioprine really equivalent for treating severe atopic eczema?
Authors: H.C. Williams
Journal: British Journal of Dermatology (2012)

Journal Article Commentary: are methotrexate and azathioprine really equivalent for treating severe atopic eczema? Get access H.C. Williams H.C. Williams Centre of Evidence‐Based Dermatology, University of Nottingham,Nottingham, NG7 2UH, U.K. E‐mail: hywel.williams@nottingham.ac.uk Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 166, Issue 4, 1 April 2012, Pages 705–707, https://doi.org/10.1111/j.1365-2133.2012.10873.x Published: 01 April 2012
Epstein-Barr Virus (EBV)-Specific Cytotoxic T Lymphocytes for the Treatment of Patients With EBV-Positive Relapsed Hodgkin's Disease
Authors: Marie A. Roskrow, Nobuhiro Suzuki, Yan-jun Gan, John W. Sixbey, Catherine Y.C. Ng, Sarah Kimbrough, Melissa Hudson, Malcolm K. Brenner, Helen E. Heslop, Cliona M. Rooney
Journal: Blood (1998)