tbuckley/cabot-search huggingface dataset:
THE COST OF TUBERCULOSIS
Authors: D T SMITH
Journal: JAMA (1921)

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
Cluster Headache
Authors: Huan J. Chang
Journal: JAMA (2009)

Cluster Headache Cluster headache was nicknamed "suicide headache" in 1939 after Dr. B. T. Horton, an American neurologist who proposed a theory for the mechanism underlying cluster headaches, described the headache as "so severe … [patients] had to be constantly watched for fear of suicide."Patients commonly describe cluster headache as the worst pain they have ever experienced.Cluster headaches are typically one-sided and tend to occur in clusters (groups) over a period of weeks or months.About 3 of 1000 people have cluster headaches.The December 9, 2009, issue of JAMA includes an article about the effectiveness of oxygen in treating cluster headaches.
New NCCN Guidelines® for Survivorship Care
Authors: Jennifer A Ligibel, Crystal S Denlinger
Journal: Journal of the National Comprehensive Cancer Network (2013)

Survivorship is a stage in the cancer journey like diagnosis and treatment, but it tends to be somewhat neglected in the quiet afterthoughts of treatment completion. Although cancer recurrence, second cancers, and late side effects of treatment are major concerns for survivors, survivors also may experience a variety of long-term physical and psychological sequelae of a cancer diagnosis and treatment. Oncology professionals may be ill-prepared to tackle these topics, and they have few guidelines for meeting these patient needs. In this article, Dr. Jennifer A. Ligibel and Dr. Crystal S. Denlinger present highlights from the inaugural NCCN Clinical Practice Guidelines in Oncology on survivorship care, focusing on the subtopics of exercise, cognitive function, immunization, and sexual function. They also discuss implementing new recommendations on survivorship assessment in the clinic.
Colorectal-Cancer Screening
Journal: New England Journal of Medicine (2012)

To the Editor: Zauber et al. (Feb. 23 issue)1 report that colonoscopic polypectomy leads to a 53% reduction in mortality. The absolute benefit to the individual patient is only about 1%. The absolute reduction may even be smaller if we account for the lower all-cause mortality observed in the treatment group. Absolute reductions in mortality are important considerations as individual patients and society as a whole weigh the benefits of screening procedures.
Differential response of prostate cancer cells to ionizing radiation: The RB status.
Authors: Robert Benjamin Den, Steve Ciment, Ankur Sharma, Hestia Mellert, Steven McMahon, Adam Dicker, Karen E. Knudsen
Journal: Journal of Clinical Oncology (2012)

106 Background: Prostate cancer is the most frequently diagnosed malignancy and the second leading cause of cancer death in U.S. men. The retinoblastoma tumor suppressor protein, RB, plays a critical role in cell cycle regulation and loss of RB has been observed in 25-30% of prostate cancers. We have previously shown that RB loss results in a castrate resistant phenotype, however the consequences of RB status with regard to radiation response are unknown. We hypothesized that RB loss would downregulate the G1-S cell cycle checkpoint arrest normally induced by irradiation, inhibit DNA repair, and subsequently sensitize cells to ionizing radiation. Methods: Experimental work was performed with multiple isogenic prostate cancer cell lines (hormone sensitive: LNCaP and LAP-C4 cells and hormone resistant C42, 22Rv1 cells; stable knockdown of RB using shRNA). Gamma H2AX assays were used to quantitate DNA damage and PARP cleavage and Caspase 3 were used to quantitate apoptosis. FACS analysis with BrdU was used to assess the cell cycle. Cell survival was measured using the clonogenic cell survival assay. In vivo work was performed in nude mice with tumor xenografts. Results: We observed that loss of RB increased radioresponsiveness in both transient and clonogenic cell survival assays in both hormone sensitive and castrate resistant cell lines (p&lt;0.05). Cell death was not mediated through increased apoptosis nor was perturbations in cell cycle noted. However, loss of RB effected DNA repair as measured by gamma H2AX staining as well as cellular senescence. In vivo xenografts of the RB deficient tumors exhibited diminished tumor mass, lower PSA kinetics and decreased tumor growth after treatment with single fraction of ionizing radiation in comparison to RB intact tumors (p&lt;0.05). Conclusions: Loss of RB results in a differential response to ionizing radiation. Isogenic cells with RB knockdown are more sensitive to DNA damage and result in reduced cell survival. The underlying mechanism appears to be related to DNA damage repair and cellular senescence.
Extrapyramidal reaction caused by ondansetron.
Authors: R B Dobrow, M A Coppock, J R Hosenpud
Journal: Journal of Clinical Oncology (1991)

Article Tools Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.1991.9.10.1921 Journal of Clinical Oncology - published online before print September 22, 2016 PMID: 1833512 Extrapyramidal reaction caused by ondansetron. R B DobrowxR B DobrowSearch for articles by this author , M A CoppockxM A CoppockSearch for articles by this author , J R HosenpudxJ R HosenpudSearch for articles by this author https://doi.org/10.1200/JCO.1991.9.10.1921 PDF "Extrapyramidal reaction caused by ondansetron.." Journal of Clinical Oncology, 9(10), p. 1921© 1991 by American Society of Clinical Oncology
Relationship Between Anaphase Aberrations and Carcinogenicity in the Trout Embryo Microinjection Assay<xref ref-type="fn" rid="FN2">2</xref>
Authors: C D Metcalfe, R A Sonstegard
Journal: JNCI Journal of the National Cancer Institute (1986)

An increased incidence of anaphase aberrations was observed in the tissues of rainbow trout embryos (Salmo gairdneri) within 96 hours of exposure to mitomycin [(MM) CAS: 50-07-7; 50 and 100 ng/embryo] and aflatoxin B1 [(AFB1) CAS: 1162-65-8; 13 and 25 ng/embryo] with the use of the trout embryo microinjection assay. High numbers of anaphase aberrations in embryos exposed to MM were associated with low mitotic indices, cell pyknosis, and high embryo mortalities. When the anaphase aberration data for embryos exposed to AFB1 were compared to previously reported carcinogenesis data from the microinjection assay, the incidence of anaphase aberrations in embryos did not show the same quantitative variations as the incidence of hepatic carcinomas in adult trout. While anaphase aberrations may be an indicator of the clastogenic effects of chemicals on fish embryos, it is unlikely that these aberrations can be used as an early indicator of a carcinogenic response in the trout embryo assay.
Abstract IA13: It takes two to tango: The PVT1-MYC alliance in human cancer
Authors: Anindya Bagchi
Journal: Cancer Research (2016)

Abstract Though gain of 8q24.21 is a common mutation in human cancers, its functional annotation is limited to studying myelocytomatosis (MYC), the prominent oncogene in the amplicon. However, MYC is co-gained with an adjacent long non-coding RNA gene plasmacytoma variant translocation 1 (PVT1), the CCDC26 gene candidate and gasdermin C GSDMC. Whether copy number gain of one or more of these genes drives neoplasia is not known. We developed chromosome engineered mouse strains with an extra copy of 1) Myc, 2) Pvt1, Ccdc26, Gsdmc, and 3) Myc, Pvt1, Ccdc26, Gsdmc. When rat Neu was introduced to test the change in the latency in mammary tumor development, only the mice with an extra copy of Myc, Pvt1, Ccdc26, Gsdmc (but not with an extra copy of Myc or Pvt1, Ccdc26, Gsdmc) developed adenocarcinomas with reduced latency, suggesting that while an extra copy of Myc gene failed to measurably advance cancer, it may co-operate with Pvt1, Ccdc26 or Gsdmc to promote cancer. Si-RNA mediated knockdown of Pvt1/PVT1 reduced the proliferation rates in the tumors, and in SK-BR-3 and MDA-MB-231, two human breast cancer cell lines with 8q24 amplification. Ablation of PVT1 markedly decreased MYC protein levels, suggesting a PVT1-dependence of MYC protein in MYC amplified cancer cells. Analysis of the cancer genome atlas suggested 99% of tumors with increased MYC copy-number also harbor co-gain of PVT1. Tissue microarray analysis revealed that PVT1 RNA and MYC protein expression are correlated in primary human tumors. These data suggests that PVT1 can potentiate MYC in human cancers. CRISPR mediated deletion of PVT1 in colorectal cell line HCT116 impaired tumor formation in xenografts, and significantly reduced MYC levels. We further confirmed the oncogenic potential of PVT1 in cancers even without supernumerary 8q24. Additionally, we have identified the putative functional domain of PVT1 which confers its oncogenic potential. We propose that the dependence of high levels of MYC on lncRNA PVT1 provides a much-needed therapeutic window against MYC protein, known to be refractory to small molecule inhibition. Citation Format: Anindya Bagchi. It takes two to tango: The PVT1-MYC alliance in human cancer. [abstract]. In: Proceedings of the AACR Special Conference on Noncoding RNAs and Cancer: Mechanisms to Medicines ; 2015 Dec 4-7; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2016;76(6 Suppl):Abstract nr IA13.
Clinical Outcomes of Metabolic Surgery: Microvascular and Macrovascular Complications
Authors: Ted D. Adams, David E. Arterburn, David M. Nathan, Robert H. Eckel
Journal: Diabetes Care (2016)

Understanding of the long-term clinical outcomes associated with bariatric surgery has recently been advanced. Research related to the sequelae of diabetes—in particular, long-term microvascular and macrovascular complications—in patients who undergo weight-loss surgery is imperative to this pursuit. While numerous randomized control trials have assessed glucose control with bariatric surgery compared with intensive medical therapy, bariatric surgery outcome data relating to microvascular and macrovascular complications have been limited to observational studies and nonrandomized clinical trials. As a result, whether bariatric surgery is associated with a long-term reduction in microvascular and macrovascular complications when compared with current intensive glycemic control therapy cannot be determined because the evidence is insufficient. However, the consistent salutary effects of bariatric surgery on diabetes remission and glycemic improvement support the opportunity (and need) to conduct high-quality studies of bariatric surgery versus intensive glucose control. This review provides relevant background information related to the treatment of diabetes, hyperglycemia, and long-term complications; reports clinical findings (to date) with bariatric surgery; and identifies ongoing research focusing on long-term vascular outcomes associated with bariatric surgery.
Polysymptomatic complaints and Briquet's syndrome in polycystic ovary disease
Authors: H Orenstein, M A Raskind, D Wyllie, W H Raskind, M R Soules
Journal: American Journal of Psychiatry (1986)

To test the hypothesis that there is an association between polycystic ovary disease and Briquet's syndrome, the authors administered a health questionnaire to infertile women with polycystic ovary disease, infertile women with tubal disease, and normal women. The patients with polycystic ovary disease endorsed significantly more physical and psychological complaints than either control group. Structured interviews revealed that five of the 39 (13%) met diagnostic criteria for definite or probable Briquet's syndrome. This study gives support to an association between polysymptomatic complaints, Briquet's syndrome, and polycystic ovary disease.
Screening for cervical cancer by direct inspection.
Authors: V. Singh, A. Sehgal, U. K. Luthra
Journal: BMJ (1992)

OBJECTIVE--To assess the efficacy of visual screening for cervical cancer in the maternal and child health setting. DESIGN--Clinical and cytological screening. SETTING--Maternal and child health centres, Delhi. SUBJECTS--44,970 women attending the centres from May 1988 to March 1991. RESULTS--238 cancers in early stages (0-IIa) were detected cytologically and proved through biopsy. Prevalence of cancer in women defined as high risk through examination by speculum was 29/1000 as compared to 1.53/1000 among women with a normal looking cervix. Though only 11.4% women belonged to the high risk category, 63% had early stage cancer. If all women with bleeding symptoms were included in the high risk category, the yield of cancer would be 71.4% (170/238) by referring only 15.6% of women attending maternal and child health centres for further evaluation through cytology or colposcopy. CONCLUSION--Though visual screening is a suboptimal strategy in comparison to the cytological screening, it may be useful where there is a heavy load of prevalent cancer and where cytological screening may not be available for years to come.
Burn Shock Therapy—Fluid Replacement First
Authors: J S MCDONALD, D E LAUGHLIN, G N BEDELL, M S BEDELL
Journal: JAMA (1964)

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
Note on the Results Obtained by Antityphoid Inoculation in the Case of an Epidemic of Typhoid Fever: Which occurred in the Richmond Asylum, Dublin
Authors: A. E. Wright
Journal: BMJ (1901)

rOT. 26, 1i¢X.e considered as evidence of even a doubtful reaction.t must, however, be noted that the precrural gland, which was already enlarged, increased considerably in size, and became tender the day after the tuberculin
Risk of Malignant Cancer Among Women With New-Onset Atrial Fibrillation
Authors: David Conen, Jorge A. Wong, Roopinder K. Sandhu, Nancy R. Cook, I-Min Lee, Julie E. Buring, Christine M. Albert
Journal: JAMA Cardiology (2016)

A substantial proportion of patients with atrial fibrillation (AF) die of noncardiovascular causes, and recent studies suggest a link between AF and cancer.To evaluate the associations between AF and cancer in a large, long-term prospective cohort study.In this cohort study, a total of 34 691 women 45 years or older and free of AF, cardiovascular disease, and cancer at baseline were prospectively followed up between 1993 and 2013, for incident AF and malignant cancer within the Women's Health Study, a randomized clinical trial of aspirin and vitamin E for the prevention of cardiovascular disease and cancer. Cox proportional hazards models using time-updated covariates were constructed to assess the association of new-onset AF with subsequent cancer and to adjust for potential confounders. Data analysis was performed from December 2014 to May 2015.New-onset AF.Incident malignant cancer confirmed by an end point committee.During a median follow-up of 19.1 years of 34 691 study participants (interquartile range [IQR], 17.6-19.7 years), new-onset AF and malignant cancer were confirmed among 1467 (4.2%) and 5130 (14.8%) participants, respectively. Median age at baseline among participants with new-onset AF and new-onset cancer during follow-up was 58 years (IQR, 52-64 years) and 55 years (IQR, 50-61 years), respectively. Atrial fibrillation was a significant risk factor for incident cancer in age-adjusted (hazard ratio [HR], 1.58; 95% CI, 1.34-1.87; P < .001) and multivariable-adjusted (HR, 1.48; 95% CI, 1.25-1.75; P < .001) models. The relative risk of cancer was highest in the first 3 months after new-onset AF (HR, 3.54; 95% CI, 2.05-6.10; P < .001) but remained significant beyond 1 year after new-onset AF (adjusted HR, 1.42; 95% CI, 1.18-1.71; P < .001), and a trend toward an increased cancer mortality was observed (adjusted HR, 1.32; 95% CI, 0.98-1.79; P = .07). In contrast, among women with new-onset cancer, the relative risk of AF was increased only within the first 3 months (HR, 4.67; 95% CI, 2.85-7.64; P < .001) but not thereafter (HR, 1.15; 95% CI, 0.95-1.39; P = .15).In this large, initially healthy cohort, women with new-onset AF had an elevated cancer risk beyond 1 year of AF diagnosis. Shared risk factors and/or common systemic disease processes might underlie this association.
Abstract IA18: Functional characterization of the tumor suppressor lysine-specific methyltransferase KMT2D in lymphoma
Authors: Ana Ortega-Molina, Isaac W. Boss, Andres Canela, Heng Pan, Yanwen Jiang, Chunying Zhao, Man Jiang, Deqing Hu, Ji-Eun Lee, Hua-Tang Chen, Daisuke Ennishi, David W. Scott, Christoffer Hother, Shichong Liu, Xing-Jun Cao, Wayne Tam, Rita Shaknovich, Benjamin A. Garcia, Randy D. Gascoyne, Kai Ge, Ali Shilatifard, Olivier Elemento, Andre Nussenzweig, Ari M. Melnick, Hans-Guido Wendel
Journal: Cancer Research (2016)

Abstract Genomic studies have revealed surprising new insights into the genetics of human B-cell lymphomas. Of particular note the lysine-specific methyl transferase KMT2D has emerged as one of the most frequently mutated genes in follicular lymphoma (FL) and in diffuse large B-cell lymphoma (DLBCL). However, the biological consequences of KMT2D mutations in lymphoma are not known. Here we show that KMT2D functions as a bona fide tumor suppressor and promotes lymphoma development in vivo. Integrative analyses of KMT2D function indicate specific and focal effects on H3K4 methylation and gene expression. These include B-cell growth and differentiation signals such as the CD40, JAK/STAT, and B-cell receptor pathways. Moreover, KMT2D targets include frequently mutated tumor suppressor genes such as TNFAIP3/A20, SOCS3, and TNFRSF14/HVEM. In this manner, KMT2D deficiency disrupts the physiological process of B-cell differentiation, facilitates malignant outgrowth, and can impede therapies acting on the CD40 and B-cell receptor pathways. Citation Format: Ana Ortega-Molina, Isaac W. Boss, Andres Canela, Heng Pan, Yanwen Jiang, Chunying Zhao, Man Jiang, Deqing Hu, Ji-Eun Lee, Hua-Tang Chen, Daisuke Ennishi, David W. Scott, Christoffer Hother, Shichong Liu, Xing-Jun Cao, Wayne Tam, Rita Shaknovich, Benjamin A. Garcia, Randy D. Gascoyne, Kai Ge, Ali Shilatifard, Olivier Elemento, Andre Nussenzweig, Ari M. Melnick, Hans-Guido Wendel. Functional characterization of the tumor suppressor lysine-specific methyltransferase KMT2D in lymphoma. [abstract]. In: Proceedings of the AACR Special Conference on Chromatin and Epigenetics in Cancer; Sep 24-27, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2016;76(2 Suppl):Abstract nr IA18.
Comparative efficacy of selective serotonin reuptake inhibitors and tricyclics in the treatment of melancholia
Authors: S P Roose, A H Glassman, E Attia, S Woodring
Journal: American Journal of Psychiatry (1994)

The popularity of selective serotonin reuptake inhibitors stems from their apparent efficacy for numerous disorders and their favorable side effect profile. However, several studies have suggested that selective serotonin reuptake inhibitors may be relatively ineffective for treating melancholia. The objective of this study was to compare the responses to fluoxetine and nortriptyline of older patients with both severe depression and heart disease.The outcome of 22 hospitalized patients with unipolar depression and heart disease who were treated with fluoxetine was compared to the outcome of 42 comparable patients treated with nortriptyline. The average age of the fluoxetine group was 73 years, and their mean pretreatment score on the Hamilton Depression Rating Scale was 26; the average age of the nortriptyline group was 70, and their mean pretreatment Hamilton score was 28.Of the 42 nortriptyline-treated patients, 28 were responders, six were nonresponders, and eight dropped out. The intent-to-treat response rate was 67% (28 of 42), and the response rate of the melancholic patients who completed the nortriptyline trial was 83% (20 of 24). Of the 22 fluoxetine-treated patients, five were responders, 13 were nonresponders, and four dropped out. The intent-to-treat response rate was 23% (five of 22), and the response rate of the melancholic patients who completed the fluoxetine trial was 10% (one of 10).Fluoxetine appears to be significantly less effective than nortriptyline for treating hospitalized elderly patients with unipolar major affective disorder, especially those with the melancholic subtype and concurrent cardiovascular disease.