tbuckley/cabot-search huggingface dataset:
BOOK REVIEWS
Authors: MICHAEL C. PERRY
Journal: JNCI Journal of the National Cancer Institute (1994)

BOOK REVIEWS Get access Cancer Medicine, Third Edition, Vols. 1 and 2 James F. Holland , Emil Frei , Robert C. Bast , Donald W. Kufe , Donald L. Morton , Ralph R. Weichselbaum , eds. Philadelphia : Lea & Febiger , 1993 . 2658 pp., illus. $195. ISBN 0812114221Cancer: Principles and Practice of Oncology, Fourth Edition, Vols. 1 and 2 Vincent T. DeVita , Samuel Hellman , Steven A. Rosenberg , eds. Philadelphia : J. B. Lippincott , 1993 . 2855 pp., illus. $225. ISBN 0397513216 MICHAEL C. PERRY MICHAEL C. PERRY Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 86, Issue 7, 6 April 1994, Page 555, https://doi.org/10.1093/jnci/86.7.555 Published: 06 April 1994
Influence of human leukocyte antigen matching on liver allograft survival and rejection: “The dualistic effect”
Authors: P Donaldson
Journal: Hepatology (1993)

To date only one published large series of human leukocyte antigen matching and liver allograft survival exists, and considerable confusion has arisen about the advantage or disadvantage of human leukocyte antigen matching. In the present study we have reinvestigated the relationship between human leukocyte antigen mismatch and graft survival in 466 first liver allografts, seeking to clarify the relationship between human leukocyte antigen and both acute rejection and the vanishing bile duct syndrome. In view of current criticism regarding the accuracy of serological tissue typing for human leukocyte antigen-DR, we have used both classic serology and restriction fragment length polymorphism analysis to ensure the accurate assignment of recipient DR types. In addition, we have used polymerase chain reaction amplification and allele-specific and sequence-specific oligonucleotide probes to retest the hypothesis that human leukocyte antigen class II matching may increase susceptibility to the vanishing bile duct syndrome. One-year graft survival was significantly lower in patients with zero or two human leukocyte antigen-A mismatches (52% and 63%, respectively) than in those with one human leukocyte antigen-A mismatch (69%) (p = 0.016 and p = 0.018). A similar effect of B mismatching was observed, with a 1-yr graft survival of 73% for those with one compared with 60% for those with two human leukocyte antigen-B mismatches. In contrast no correlation was found between DR mismatch and graft survival. Human leukocyte antigen class I matching appears to influence graft survival largely through the occurrence of acute rejection and the development of the vanishing bile duct syndrome. In those patients who underwent liver biopsies, 49% (28 of 57) without acute rejection had a single B mismatch compared with 32% (88 of 263) with acute rejection (x2 = 5.5, p < 0.025). In addition, a complete human leukocyte antigen-A mismatch was more common in those who developed the vanishing bile duct syndrome than in those with normal graft function (54% vs. 38%; X2 = 4.26, p < 0.05). In contrast to previous reports from this unit, no relationship between human leukocyte antigen-DR or -DQ mismatch and the vanishing bile duct syndrome could be detected. These findings indicate that human leukocyte antigen class I compatibility exerts a dual effect on the survival of primary liver allografts. Although some human leukocyte antigen-A and –B matching may be desirable for liver transplantation, full class I matching may have an adverse effect. (HEPATOLOGY 1993;17:1008–1015.)
Effect of LDL-apheresis on coronary plaque characteristics in patients with familial hypercholesterolemia assessed by intravascular ultrasound with wavelet analysis Takafumi Hiro, Katsuhiko Hiramori, Akira Kitabatake, Tsutomu Imaizumi, Hitoshi Hishida, Masanori Nomura, Ichiro Sakuma, Kenichi Fukami, Takashi Honda, Hiroshi Ogawa, Takashi Fujii, Masunori Matsuzaki. Yamaguchi University, Ube, Japan
Journal: Journal of the American College of Cardiology (2001)
The Bottle Fighters.
Journal: JAMA (1963)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Abstract A2-49: Integrated Omic analysis of lung cancer reveals metabolism proteome signatures with prognostic impact
Authors: Michael F. Moran, Thomas Kislinger, Lei Li, Vladimir Ignatchenko, Yuhong Wei, Christine To, Paul Taylor, Jiefei Tong, Nhu An Pham, Melania Pintilie, Lakshmi Muthuswamy, Frances A. Shepherd, Ming Sound Tsao
Journal: Cancer Research (2015)

Abstract Cancer results from processes prone to selective pressure and dysregulation acting along the sequence-to-phenotype continuum DNA→RNA→Protein→Disease. An Omics Array integrating DNA gene copy number, mRNA transcriptome, and quantified proteome was assembled into a genetic map representing non-small cell lung carcinoma (NSCLC). Data were collected from patient-matched normal lung, primary tumors, and patient tumor-derived xenograft (PDX) tumors. Dysregulated proteins not previously implicated as cancer drivers were found encoded throughout the genome including but not limited to regions of recurrent DNA amplification/deletion in NSCLC. Unsupervised clustering revealed signatures comprising metabolism proteins particularly highly recapitulated between matched primary and PDX tumors, and which distinguished between the major NSCLC histological subtypes adenocarcinoma (ADC) and squamous cell carcinoma (SCC). Interrogation of The Cancer Genome Atlas (TCGA) revealed sizeable cohorts of NSCLC patients with DNA alterations in genes encoding the metabolism proteome signatures, and accompanied by differences in survival. Similar to the proteome signatures from which they were extrapolated, the gene mutation signatures with prognostic impact discriminated between the lung ADC and SCC subtypes. Serine hydroxymethyltransferase 2 (SHMT2), a key enzyme in serine/glycine and folate-dependent one-carbon metabolism, is upregulated in the proteomes of NSCLC primary and PDX tumours, and is implicated as a driver of recurrent chromosome 12q14.1 amplification in NSCLC. SHMT2, along with other enzymes implicated as anti-folate targets, is also part of a metabolism signature associated with poor outcome in lung ADC. The interrogation of cancer genomes and proteomes for alterations that are related products of selective pressures driving the cancer phenotype may be a general approach to uncover and group together cryptic, polygenic cancer drivers, which might represent new anti-cancer therapeutic targets. Note: This abstract was not presented at the conference. Citation Format: Michael F. Moran, Thomas Kislinger, Lei Li, Vladimir Ignatchenko, Yuhong Wei, Christine To, Paul Taylor, Jiefei Tong, Nhu An Pham, Melania Pintilie, Lakshmi Muthuswamy, Frances A. Shepherd, Ming Sound Tsao. Integrated Omic analysis of lung cancer reveals metabolism proteome signatures with prognostic impact. [abstract]. In: Proceedings of the AACR Special Conference on Translation of the Cancer Genome; Feb 7-9, 2015; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2015;75(22 Suppl 1):Abstract nr A2-49.
Chloroquine and Nonconvulsive Status Epilepticus
Authors: Paul Mulhauser
Journal: Annals of Internal Medicine (1996)

Letters15 March 1996Chloroquine and Nonconvulsive Status EpilepticusPaul Mulhauser, MD, Yves Allemann, MD, and Claude Regamey, MDPaul Mulhauser, MDHopital Cantonal; 1708 Fribourg; SwitzerlandSearch for more papers by this author, Yves Allemann, MDHopital Cantonal; 1708 Fribourg; SwitzerlandSearch for more papers by this author, and Claude Regamey, MDHopital Cantonal; 1708 Fribourg; SwitzerlandSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-124-6-199603150-00021 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:We thank Drs. Benbadis and Van Ness for allowing us to clarify the concept of nonconvulsive status epilepticus. This classification depends on the degree of importance given to clinical signs when defining partial complex status epilepticus and absence status. Some authors claim that it is impossible to differentiate among the various forms of nonconvulsive status epilepticus on clinical grounds [1, 2], whereas others have established criteria for precisely that purpose [3]. Furthermore, Cascino [4] defines two subgroups of complex partial status epilepticus: type I, with repeated but focal EEG alterations, and type II, with either continuous partial or ...References1. Lugarcsi E, Pazzaglia P, Tassinari CA. Differentiation of “absence status” and “temporal lobe status.” Epilepsia. 1971; 12:77-87. Google Scholar2. Porter RJ, Penry JK. Petit mal status. In: Delgads-Escueta AV, Wasterlain CG, Treiman DM, Porter RJ, eds. Advances in Neurology. New York: Raven; 1983:61-70. Google Scholar3. Rohr-Le Floch J, Gauthier G, Beaumanoir A. Confusional states of epileptic origin. Value of emergency EEG. Rev Neurol (Paris). 1988; 144:6-7, 425-36. Google Scholar4. Cascino G. Nonconvulsive status epilepticus in adults and children. Epilepsia. 1993; 34(Suppl 1):21-8. Google Scholar Author, Article, and Disclosure InformationAuthors: Paul Mulhauser, MD; Yves Allemann, MD; Claude Regamey, MDAffiliations: Hopital Cantonal; 1708 Fribourg; Switzerland PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 March 1996Volume 124, Issue 6Page: 615KeywordsChloroquineElectroencephalographyEpilepsyEpileptic seizuresStatus epilepticus ePublished: 15 August 2000 Issue Published: 15 March 1996 Copyright & PermissionsCopyright © 1996 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Danger of instant adhesives.
Authors: C P de Fonseka
Journal: BMJ (1976)

Diet and the diabetic SIR,-We wish to comment on your leading article on this subject (2 October, p 781) and to report briefly the opinion of most paediatric diabetologists.We are often in disagreement with the dietetic management recommended by diabetologists concerned with diabetic adults.As we are not permitted free expression within the International Diabetes Federation, we formed, in 1972, the International Study Group of Diabetes in Children and Adolescents.Although we have representatives of 13 countries, unfortunately Great Britain is not yet included.We therefore take this opportunity to invite our British colleagues to join us so that we may work together in this study group.It is evident that both paediatricians and internists concerned with diabetes in childhood are trying to establish the best possible degree of metabolic control'-that is, minimum glycosuria, normal blood lipids, avoidance of hypo-and hyper-glycaemia (which is a factor in the development of angiopachy), and normal growth.2We have shown by angiofluorography that in children there exists a correlation between diabetic retinopathy and degree of
Mislabelled Agar-Gel Plate
Journal: JAMA (1969)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
THE GIANT CELL IN HEALING TUBERCULOSIS.
Journal: JAMA (1898)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Editorial board
Authors: Gail Shapiro, Lanny Rosenwasser, Wash Denver, D Metcalfe, Immediate Past, William Busse, Robert Rich, James Kemp, Atlanta Ga, San Diego, Robert Bush, Louis Mendelson, West Hartford, Thomas Casale, Lawrence Schwartz, William Henderson, Seattle Wash, William Shearer, Robert Lemanske, Gillian Shepherd, New York, Gailen Marshall, Donald Leung, Colo Deputy, Harold Nelson, Stanley Szefler, Colo Associate, James Crapo, Erwin Gelfand, Gary Larsen, Bruce Bochner, Philip Norman, Kay Whalen
Journal: Journal of Allergy and Clinical Immunology (2001)
Pregnancy hormone levels signal trisomy 21, improved screening, lower costs possible
Authors: T. Randall
Journal: JAMA (1991)

ADVANCES in biochemistry are helping scientists identify pregnant women who are at high risk for carrying a fetus with Down's syndrome. Scientists now recognize three substances in the mother's serum—human chorionic gonadotropin, unconjugated estriol, and α-fetoprotein (AFP)—the concentrations of which, when coupled with the woman's age-associated risk, allow a more accurate calculation of the likelihood that she is carrying an affected fetus. The prenatal blood test, administered during the second trimester and followed by amniocentesis and chromosome analysis on those mothers who are at risk, detects about 67% of all affected fetuses in the general pregnant population—a twofold to threefold improvement from the standard screening method that employs only AFP serum levels and age-associated risk. <h3>Identifying Younger Patients</h3> The new method helps to identify younger patients who are at high risk and should have amniocentesis performed but may not be offered the procedure under standard screening methods. It can also
EPEN-52. METABOLIC REGULATION OF THE EPIGENOME DRIVES LETHAL INFANTILE EPENDYMOMA
Authors: Sachin Kumar, Antony Michealraj, Leo Kim, Jeremy Rich, Michael Taylor
Journal: Neuro-Oncology (2020)

Abstract PFA ependymomas are a lethal glial malignancy of the hindbrain found in infants and toddlers. Lacking any highly recurrent somatic mutations, PFAs have been proposed to be a largely epigenetically driven entity, defined by hypomethylation at the histone 3 lysine 27 residue. Unfortunately, an almost complete lack of model systems has limited the discovery of novel PFA therapies. In this study, we have identified that the PFA hypoxic microenvironment controls the availability of specific metabolites, resulting in diminished H3K27 trimethylation and increased H3K27 acetylation in vitro and in vivo. Unique to PFA cells, transient exposure to ambient oxygen results in irreversible cellular toxicity. Furthermore, perturbation of key metabolic pathways is sufficient to inhibit growth of PFA primary cultures in vitro. Although PFA tumors exhibit a low basal level of H3K27me3, inhibition of H3K27 methylation paradoxically demonstrates significant and specific activity against PFA. Thus, we propose a “Goldilocks Model” of metabolic-epigenetic regulation in PFA ependymoma, whereby increased or decreased H3K27 trimethylation results in cell death. Mapping of PFA ependymoma tumours suggests a cell of origin arising in the first trimester of human development where there is a known hypoxic microenvironment. Therefore, targeting metabolism and/or the epigenome presents a unique opportunity for rational therapy for infants with PFA ependymoma.
Alcohol and family violence
Authors: I. Schwartz
Journal: JAMA (1989)

<h3>In Reply.—</h3> Several individuals have called our attention to an unfortunate error in typing that led to publication of an incorrect Table 1. The correct version, as they have all pointed out, is as shown (Table). Drs Woodruff and Baron make an important point in noting that predictive values (which we termed<i>clinical accuracy</i>in an attempt to make it more understandable to those not expert in decision theory) are sensitive to changes in prevalence. As a matter of fact, predictive values were added to the manuscript in response to the suggestion of one of the reviewers, who remarked that their use would be acceptable, so long as they were not going to be directly applied in the screening of other populations. In some of the diseases we studied, there was a marked change inprevalence (as in the case of tuberculosis) that accounted for much of the change in
STATE SOCIETY AUXILIARY COMMITTEE.
Journal: JAMA (1906)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
INFANTILE CEREBRAL PALSY AND EPILEPSY.
Journal: JAMA (1899)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Infographic. What interventions can improve quality of life or psychosocial factors of individuals with knee osteoarthritis? A systematic review with meta-analysis of primary outcomes from randomised controlled trials
Authors: Ronaldo Valdir Briani, Amanda Schenatto Ferreira, Marcella Ferraz Pazzinatto, Evangelos Pappas, Danilo De Oliveira Silva, Fábio Mícolis de Azevedo
Journal: British Journal of Sports Medicine (2018)
Incidence of Pulmonary Embolism as Indicator of Value of Thrombosis Prophylaxis: Four Years' Experience with Thrombodym (Neodymium-Sulfoisonicotinate)
Journal: JAMA (1963)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal