tbuckley/cabot-search huggingface dataset:
Radiation Therapy in New Hampshire, Massachusetts and Rhode Island
Authors: Bernard S. Bloom, Osler L. Peterson, Samuel P. Martin
Journal: New England Journal of Medicine (1972)

Abstract There are large variations in input, output and cost of radiation therapy among different categories of hospitals. Hospitals with similar patient loads exhibit similar investment, staffing patterns and disease mix. The use of facilities, equipment and staff in low-patient-load hospitals is less intensive and includes a high proportion of benign conditions. The high-patient-load centers make more intensive use of their resources and treat a far higher proportion of patients with cancer, and the therapy provided is more expensive. The greater cost is due mainly to the larger and more diversified staff administering radiation therapy. Five major centers could provide the necessary radiation therapy in the area studied. The cost would probably be higher, but the results could well be superior.
Analyses of mating differences within-sex and between-sex are complementary, not competing
Authors: Todd K. Shackelford, Gregory J. LeBlanc, Richard L. Michalski, Viviana A. Weekes
Journal: Behavioral and Brain Sciences (2000)

Analyses of between-sex differences have provided a powerful starting point for evolutionarily informed work on human sexuality. This early work set the stage for an evolutionary analysis of within-sex differences in human sexuality. A comprehensive theory of human sexual strategies must address both between-sex differences and within-sex differences in evolved psychology and manifest behavior.
A novel function of CD40: induction of cell death in transformed cells.
Authors: S Hess, H Engelmann
Journal: The Journal of Experimental Medicine (1996)

CD40 is known as an important T-B cell interaction molecule which rescues B lymphocytes from undergoing apoptosis. Like other receptors of the tumor necrosis factor (TNF) receptor gene family, CD40 is expressed on cells of different tissue origins including some transformed cells. In contrast to its well-studied effects on B cells, the biological functions of CD40 in non-immune cells remain largely unknown. Here we show that CD40 ligation induces apoptotic cell death in transformed cells of mesenchymal and epithelial origin. This CD40-mediated cell death seems to use a preformed signaling pathway since it occurs even when protein synthesis is blocked. Notably, the CD40 cytoplasmic domain shares a structural homology with the recently defined "death domains" of the 55-kD TNF receptor (p55TNFR) and Fas. Despite these structural similarities, differences are seen in the way phorbol myristate acetate, interleukin 1, TNF, and various metabolic inhibitors influence the cellular responsiveness to CD40, p55TNFR, and Fas-mediated killing. Our study indicates that CD40 induces cell death by a distinct mechanism.
Hepatic Impairment During the Intake of Contraceptive Pills: Clinical Trial with Postmenopausal Women
Authors: A. Eisalo, P. A. Jarvinen, T. Luukkainen
Journal: BMJ (1964)

12 postmenopausal women were given Lyndiol for 28 days (7 women) Or gametril (2 women) or Mestranol (3 women).  Hepatic function was studie d.  In every patient receiving Lyndiol the transaminase level in the serum was clearly elevated after 20 days.  Bromsulphthalein retention and clearance showed highly pathological values in 3 women.  1 woman had elevated total bilirubin.  Orgametril the progestogen component of Lyndiol did not seem to result in any abnormal liver function.  The estrogen component (Mestranol) resulted in raised serum transaminase levels and bromsulphthalein retention in 1 patient of 3.  It is concluded that the estrogen component may be responsible for the changes in liver function.
Professionalism in Medicine: Critical Perspectives
Authors: Alice Z. Frohna
Journal: JAMA (2007)

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
Hemolytic Anemia and G-6-PD Deficiency
Authors: Paul G. Hattersley
Journal: JAMA (1969)

<h3>To the Editor:—</h3> I noted with considerable interest your editorial comment, "Hemolytic Anemia Complicating Viral Hepatitis and G-6-PD Deficiency" (<b>208</b>:2468, 1969), and particularly your reference to two reports of acute renal shut-down in such patients. I wonder whether your warning of the dangers of renal complications in patients with this enzyme defect should not be extended to those with virus disorders other than hepatitis. I should like to report briefly a patient who, because of massive intravascular hemolysis, was considered to be in great danger of intravascular coagulation, with possible kidney damage, and who received heparin without waiting for evidences of coagulation. <h3>Report of a Case:—</h3> A 17-month-old boy of Greek-American extraction woke one morning appearing pale and listless, and with his wet diapers stained deep red. The patient had had a small-pox vaccination four days before, and had had an upper-respiratory tract infection for the prior two days.
Muscarinic Cholinergic Antagonism Does Not Enhance Recovery From Hypoglycemia in IDDM
Authors: Annemarie Hvidberg, Philip E Cryer
Journal: Diabetes Care (1995)

OBJECTIVE Because muscarinic cholinergic agonism in the absence of an increase in glucagon secretion inhibits hepatic glucose production, we tested the hypothesis that muscarinic cholinergic antagonism enhances glucose recovery from hypoglycemia in insulin-dependent diabetes mellitus (IDDM). RESEARCH DESIGN AND METHODS Eight (initially euglycemic) patients with IDDM received overnight infusions of insulin and were studied on three occasions in random order. Hypoglycemia was induced by low-dose insulin infusion (4.0 pmol·kg−1 min−1) from 0 through 80 min; observations were continued through 240 min. At 0 and 80 min, intravenous injections of atropine only (1.0 mg), placebo and then atropine, respectively, or placebo only were administered. RESULTS Increments in heart rate (P &amp;lt; 0.001) and prevention of the pancreatic polypeptide response to hypoglycemia (P = 0.042) after atropine administration documented muscarinic cholinergic antagonism. The absent glucagon response to hypoglycemia was unaltered, but the epinephrine response was increased (P = 0.010). Nonetheless, rates of glucose production and utilization and plasma glucose concentrations were unaltered. CONCLUSIONS We conclude that muscarinic cholinergic antagonism does not enhance glucose recovery from hypoglycemia in patients with IDDM.
TCT-40 10 mg/L of high-sensitivity C-reactive protein on admission is a powerful predictive marker in patients with ST-segment elevation myocardial infarction, but not in patients with non-ST-segment elevation myocardial infarction
Authors: Sungmin Lim, Byung-Hee Hwang, Hee-Yeol Kim, Kiyuk Chang, Myung Ho Jeong, Ki-Bae Seung
Journal: Journal of the American College of Cardiology (2014)
Mandatory Cancer Risk Warnings on Alcoholic Beverages: What Are the Ethical Issues?
Authors: Jennie Louise, Jaklin Eliott, Ian Olver, Annette Braunack-Mayer
Journal: The American Journal of Bioethics (2015)

The link between alcohol consumption and cancer is well established, but public awareness of the risk remains low. Mandated warning labels have been suggested as a way of ensuring "informed choice" about alcohol consumption. In this article we explore various ethical issues that may arise in connection with cancer warning labels on alcoholic beverages; in particular we highlight the potentially questionable autonomy of alcohol consumption decisions (either with or without labels) and consider the implications if the autonomy of drinking behavior is substantially compromised. Our discussion demonstrates the need for the various ethical issues to be considered and addressed in any decision to mandate cancer warning labels.
Human T cells respond to mouse mammary tumor virus-encoded superantigen: V beta restriction and conserved evolutionary features.
Authors: N Labrecque, H McGrath, M Subramanyam, B T Huber, R P Sékaly
Journal: The Journal of Experimental Medicine (1993)

Mouse mammary tumor virus (MMTV)-encoded superantigens (SAGs) influence the murine T cell repertoire and stimulate a strong mixed lymphocyte response in vitro. These SAGs are encoded by the open reading frame of the 3' long terminal repeat of MMTV, termed MMTV SAGs. The T cell response to MMTV SAGs is V beta restricted and requires expression of the class II molecules of the major histocompatibility complex (MHC) on the presenting cells. While human T cells respond to bacterial SAGs, it is not known if human T cells or human MHC class II molecules can interact with MMTV SAGs. A fibroblastic cell line expressing the human MHC class II molecule HLA-DR1 and the Mtv-7 sag gene encoding Mls-1 was used to stimulate human T cells. We show here that human T cells efficiently proliferate in response to Mls-1 presented by HLA-DR1. This T cell response was inhibited by mAbs directed against CD4 or MHC class II molecules but not by mAbs specific for CD8 or MHC class I molecules. Moreover, the response to Mls-1 was limited to human T cells expressing a restricted set of T cell receptor V beta chains. Human T cells expressing V beta 12, 13, 14, 15, and 23 were selectively amplified after Mtv-7 sag stimulation. Interestingly, these human V beta s share the highest degree of homology with the mouse V beta s interacting with Mls-1. These results show a strong evolutionary conservation of the structures required for the presentation and the response to retrovirally encoded endogenous SAGs, raising the possibility that similar elements operate in humans to shape the T cell repertoire.
Ibuprofen is a marker of soft tissue infection
Authors: N. D Moore
Journal: BMJ (2008)

The references cited in Ospina and Salcedo’s letter seem not to support the authors’ affirmation that ibuprofen increases the risk of soft tissue infection in varicella.1 Reference 3—the only methodologically sound study—says that the study data do not support the hypothesis that non-steroidal anti-inflammatory drugs, or ibuprofen in particular, increase the risk …
Hospital bed utilisation in the NHS and Kaiser Permanente
Authors: David A Evans
Journal: BMJ (2004)

Editor—The article by Feachem et al comparing Kaiser with the NHS attracted much attention, not least from the Department of Health.1 However, the authority of the debate is diluted by the way in which the article by Ham et al was published.2

Firstly, Ham did not declare any competing interests. The Department of Health, for which he is strategy director, is currently running pilot studies in seven primary care trusts, adapting elements of the Kaiser model. He therefore has a vested interest in showing that the model his team has advocated performs better than the NHS.

Secondly, the conclusions of the paper were presented as fact in the summary box “What this study adds.” The paper implies that Kaiser has accomplished its better acute bed utilisation through integration of care, active management of patients, and the use of intermediate care, self care, and medical leadership. Neither it nor Feachem et al's paper present any evidence that this is the case: these claims are either speculative or based on their own analysis of the Kaiser system. Whether Kaiser achieves better bed utilisation and how this is achieved has not been conclusively shown.

The presentation of the paper in this way does not promote debate but weakens it. The Department of Health set up pilots modelled on aspects of the Kaiser system on the basis of Feachem et al's flawed article, which was surely intended only to initiate debate. Unsubstantiated conclusions should not be presented as fact to fuel another fruitless political exercise.

Unfortunately, the primary care trust pilots will all omit the most important distinction of the Kaiser system—that it is not run by politicians.
Methylation-Associated Silencing of the<i>Nuclear Receptor 1I2</i>Gene in Advanced-Type Neuroblastomas, Identified by Bacterial Artificial Chromosome Array-Based Methylated CpG Island Amplification
Authors: Akiko Misawa, Jun Inoue, Yuriko Sugino, Hajime Hosoi, Tohru Sugimoto, Fumie Hosoda, Misao Ohki, Issei Imoto, Johji Inazawa
Journal: Cancer Research (2005)

Abstract To identify genes whose expression patterns are altered by methylation of DNA, we established a method for scanning human genomes for methylated DNA sequences, namely bacterial artificial chromosome array-based methylated CpG island amplification (BAMCA). In the course of a program using BAMCA to screen neuroblastoma cell lines for aberrant DNA methylation compared with stage I primary neuroblastoma tumors, we identified CpG methylation-dependent silencing of the nuclear receptor 1I2 (NR1I2) gene. NR1I2 was methylated in a subset of neuroblastoma cell lines and also in advanced-stage primary tumors with amplification of MYCN. Its methylation status was inversely associated with gene expression. Treatment with the demethylating agent 5-aza-2′-deoxycytidine restored NR1I2 transcription in neuroblastoma cell lines lacking endogenous expression of this gene. A CpG island located around exon 3 of NR1I2 showed promoter activity, and its methylation status was clearly and inversely correlated with NR1I2 expression status. The gene product, NR1I2, has a known function in regulating response to xenobiotic agents but it also suppressed growth of neuroblastoma cells in our experiments. We identified some possible transcriptional targets of NR1I2 by expression array analysis. The high prevalence of NR1I2 silencing by methylation in aggressive neuroblastomas, together with the growth-suppressive activity of NR1I2, suggests that this molecule could serve as a diagnostic marker to predict prognosis for neuroblastomas.
Extracellular proton release by stimulated neutrophils.
Authors: R van Zwieten, R Wever, M N Hamers, R S Weening, D Roos
Journal: Journal of Clinical Investigation (1981)

We have tried to elucidate the mechanism of phagosome acidification in human neutrophils. Assuming that phenomena occurring at the plasma membrane reflect reactions in the phagocytic vacuoles, we have stimulated human neutrophils with agents that induce a "respiratory burst," and we have measured the release of protons into the extracellular medium. Phorbol myristate acetate, N-formyl-methionyl-leucyl-phenylalanine and serum-opsonized zymosan particles each caused a rapid release of protons, concomitant with the increase in oxygen consumption. The stimulated release of protons was strictly coupled to the increase respiration of the cells, because inhibition of the respiration of either anaerobiosis, chlorpromazine, or glycolytic inhibitors also inhibited the release of protons. Also, in the presence of the above-mentioned stimulating agents, neutrophils from three patients with chronic granulomatous disease enhanced neither respiration not proton release. In normal cells, the ratio of deltaH+/-deltaO2 was 1.04 +/- 0.19 (mean +/ SD, n = 13). The mechanism of this proton release is not clear. The amount of lactic and carbonic acid produced by stimulated neutrophils was inadequate to explain the amount of protons released. Perhydroxyl radicals were also ruled out as the source of the protons. Because the cells did not release measurable amounts of phosphate ions, a phosphate-hydroxyl-ion antiport was also excluded. Finally, the lack of any effect of uncouplers renders it unlikely that a respiration-driven proton gradient is built up across the plasma membrane.
Immunoglobulin M levels inversely correlate with CD40 ligand promoter methylation in patients with primary biliary cirrhosis
Authors: Ana Lleo, Jieyue Liao, Pietro Invernizzi, Ming Zhao, Francesca Bernuzzi, Le Ma, Gaetana Lanzi, Aftab A. Ansari, Ross L. Coppel, Peng Zhang, Yijun Li, Zhiguang Zhou, Qianjin Lu, Eric M. Gershwin
Journal: Hepatology (2011)

The cross-talk of cluster of differentiation (CD)40/CD40 ligand (CD40L) plays a key role in CD4(+) T-cell priming, B-cell terminal maturation, and immunoglobulin (Ig) class-switch recombination. Genetic defects in the CD40L lead to a disorder characterized by elevated concentrations of serum IgM and immunodeficiency. Patients with primary biliary cirrhosis (PBC) characteristically show circulating antimitochondrial antibodies (AMAs), liver-infiltrating autoreactive T lymphocytes against mitochondrial antigens, and high levels of IgM. We hypothesized that CD40L may play a key role in the pathogenesis of the elevated serum IgM and analyzed genetic and epigenetic modifications of the gene coding for CD40L in CD4(+) and CD8(+) T cells isolated from circulating mononuclear cells from PBC patients and healthy controls. We herein demonstrate significantly lower levels of DNA methylation of the CD40L promoter in CD4(+) T cells from PBC patients, as compared with controls, and this decreased methylation was inversely correlated with levels of serum IgM in PBC patients.The findings of an absence of genetic modifications of the CD40L gene, in concert with decreased DNA methylation of the CD40L promoter in PBC patients, suggests that environmental factors, rather than genetics, must play a major role in the pathogenesis of elevated serum IgM in PBC.
Similar evolutionary patterning among repeated and single copy nematode mitochondrial genes
Authors: B. C. Hyman, J. L. Azevedo
Journal: Molecular Biology and Evolution (1996)

Ten of 12 mitochondrial protein-coding genes and the large (16S) mitochondrial rRNA gene have been identified and mapped within the Romanomermis culicivorax mitochondrial genome. This transcriptional map differs from other nematode mitochondrial DNAs (mtDNAs) with respect to gene order and transcriptional orientation of some genes. Several of these coding regions are components of a 3.0-kilobase mtDNA repeating unit, allowing a direct comparison of nucleotide and amino acid sequence composition for repeated and single copy genes. Analysis of protein-coding regions representing repeated (ND3, ND6) and single copy genes (ATPase 6, cyt.b, COI, COIII, ND1, ND4, ND5), and four repeat-associated open reading frames (ORFs) with unassigned function have revealed striking similarities in nucleotide composition, amino acid frequencies, and codon biases. Although we anticipated that reiterated protein coding regions might be evolving under relaxed selection, our results indicate that both repeated and unique mitochondrial genes appear subject to similar functional constraints.
STUDIES IN THE COMMON COLD
Authors: Katherine C. Mills, G. S. Shibley, A. R. Dochez
Journal: The Journal of Experimental Medicine (1928)

1. A study of the Gram-negative, filter-passing, anaerobic organisms, described by Olitsky and Gates, and Gates and McCartney, has been undertaken with a view to determining their general character and their possible rôle in the causation of the common cold. 2. These organisms seem to constitute part of the normal flora of the upper respiratory tract and would seem to bear no etiological relationship to the common cold.
Sex bias in the management of coronary artery disease
Authors: Richard Steingart, Milton Packer, Marrick Kukin, Peggy Hamm, Lem Moye, MaryEllen Coglianese, Josephine Sollano, Sandra Lewis, Bernard Gersh, Edward Geltman, Niki Kantrowitz, Stanley Katz, Marc Pfeffer
Journal: Journal of the American College of Cardiology (1990)
The Effect of Acute Alcohol Intoxication and Chronic Alcohol Abuse on Outcome From Trauma
Authors: Gregory J. Jurkovich
Journal: JAMA (1993)

To determine the effect of acute alcohol intoxication and chronic alcohol abuse on morbidity and mortality from trauma.Prospective cohort study.Blunt or penetrating trauma patients at least 18 years of age admitted to one trauma center or dying at the injury scene.Mortality, complications (infection, pneumonia, respiratory failure, or multiple organ failure), and length of hospital stay.Acute intoxication had no effect on risk of dying--at the injury scene, within the first 24 hours of hospitalization, after the first 24 hours, or overall. Acute intoxication also did not increase the risk of complications and was associated with shorter lengths of stay. Patients with both biochemical and behavioral evidence of chronic alcohol abuse had a twofold increased risk of complications, particularly pneumonia and any infection, compared with those with no evidence of chronic alcohol abuse.Chronic, but not acute, alcohol abuse adversely affects outcome from trauma. Attention to the problem of chronic alcohol abuse in trauma patients is necessary, and screening trauma patients for chronic alcohol abuse appears to be warranted.
Somatostatin receptor-mediated tumor-targeting drug delivery using octreotide-PEG-deoxycholic acid conjugate-modified N-deoxycholic acid-O, N-hydroxyethylation chitosan micelles
Authors: Meirong Huo, Aifeng Zou, Chengli Yao, Yong Zhang, Jianping Zhou, Jing Wang, Qinnv Zhu, Jing Li, Qiang Zhang
Journal: Biomaterials (2012)
Phase I Study to Assess the Combination of Afatinib with Trastuzumab in Patients with Advanced or Metastatic HER2-Positive Breast Cancer
Authors: Alistair Ring, Duncan Wheatley, Helen Hatcher, Robert Laing, Ruth Plummer, Martina Uttenreuther-Fischer, Graham Temple, Katy Pelling, David Schnell
Journal: Clinical Cancer Research (2014)

The HER2 mAb, trastuzumab, is a standard therapy for patients with HER2-positive breast cancer before acquired resistance. Afatinib, an irreversible, oral, small-molecule ErbB family blocker, shows clinical activity in trastuzumab-refractory HER2-positive breast cancer.This phase I study used a 3+3 dose escalation to determine the MTD of oral once-daily afatinib in combination with the recommended dose of intravenous trastuzumab (4 mg/kg week 1; 2 mg/kg/wk thereafter). Adult women with confirmed advanced/metastatic HER2-positive breast cancer were eligible.Of 18 patients treated, 16 received daily afatinib 20 mg and two 30 mg. Overall, 4 of 13 and 2 of 2 patients receiving afatinib 20 mg and 30 mg, respectively, experienced dose-limiting toxicity (DLT; all CTCAE grade 3 diarrhea). Most frequent treatment-related adverse events were diarrhea (94%), rash (56%), and fatigue (56%). Overall, pharmacokinetic profiles of afatinib and trastuzumab in combination were consistent with the known characteristics of each alone. Overall, objective response and disease control rates were 11% and 39%, respectively, with median progression-free survival 111.0 days (95% confidence interval, 56.0-274.0).The MTD of afatinib was 20 mg daily combined with the recommended weekly dose of trastuzumab, with 1 of 6 patients showing DLTs in the dose escalation. However, additional DLTs occurred in the dose-expansion phase meaning that this MTD cannot be recommended for phase II development without strict diarrhea management. There was no evidence suggesting relevant pharmacokinetic drug-drug interactions. Signs of clinical activity were seen in trastuzumab-resistant HER2-positive breast cancer, suggesting further investigation with optimal diarrhea management is warranted.