tbuckley/cabot-search huggingface dataset:
Abstract P1-13-12: Intermittent letrozole as adjuvant treatment in postmenopausal hormone-receptor positive early breast cancer patients
Authors: A Balduzzi, V Bagnardi, S Volpe, G Cancello, M Iorfida, S Dellapasqua, M Sandri, A Goldhirsch, M Colleoni
Journal: Cancer Research (2013)

Abstract Background: Low-dose estrogen might induce apoptosis in breast cancer cells that develop resistance to antihormonal therapy. Letrozole withdrawal for 3-month might permit estrogenic stimulation in residual resistant disease susceptible to letrozole reintroduction. We investigated the impact of a 3-month letrozole free interval on serum Estradiol levels in patients with early stage breast cancer. Patients and methods: Postmenopausal women with ER and/or PgR ≥ 10% of the cells, node-negative early breast cancer were eligible. Patients (pts) received letrozole (2.5 mg daily) for five years with a 3-month treatment free interval after the 1st year of therapy. The primary endpoint was to evaluate the increase in serum estradiol absolute levels after 3-month treatment free interval. The secondary endpoints were the evaluation of others biological markers (e.g. FSH, LH, Cholesterol, HDL, triglycerides, osteocalcin). Estradiol levels were quantified by ECLIA assay that measured estradiol concentrations with a 5 pg/ml lower detection limit. FSH and LH levels (mU/ml) were measured by ECLIA assay, Osteocalcin (ng/ml) by RIA assay, Cholesterol, HDL, and Triglycerides (mg/ml) by colorimetric assay. Results: From November 2007 to February 2012, 130 evaluable pts were enrolled. The median age was 61 years. One-hundred ten pts (85%) had pT1 tumor, 88 pts (68%) presented grade 2 and 83 pts (64%) showed a Ki-67 LI &amp;lt;20%. Mean values of estradiol levels at time of discontinuation were 5.6 pg/ml (standard deviation: 1.7). Estradiol levels increased after a 3-month free interval by a mean of 3.3 pg/ml (66%; P &amp;lt;0.0001). FSH and LH levels decreased from baseline by a mean of 7.5 mU/ml (P&amp;lt;0.0001), and 1.4 mU/ml (P = 0.0062) respectively. Triglycerides decreased from baseline by a mean of 8.6 mg/dl (P = 0.036), and osteocalcin increased by a mean of 2.8 ng/ml (P = 0.013). Conclusions: Intermittent Letrozole significantly impact on estradiol levels. This study provides further evidence supporting the role of intermittent letrozole in the adjuvant treatment of postmenopausal patients with endocrine responsive breast cancer. Citation Information: Cancer Res 2013;73(24 Suppl): Abstract nr P1-13-12.
C5a-induced expression of P-selectin in endothelial cells.
Authors: K E Foreman, A A Vaporciyan, B K Bonish, M L Jones, K J Johnson, M M Glovsky, S M Eddy, P A Ward
Journal: Journal of Clinical Investigation (1994)

Human umbilical vein endothelial cells have recently been shown to respond to C5a with increases in intracellular Ca2+, production of D-myo-inositol 1,4,5-triphosphate and superoxide anion generation. In the current studies, C5a had been found to cause in a time- and dose-dependent manner rapid expression of endothelial P-selectin, secretion of von Willebrand factor, and adhesiveness for human neutrophils. The effects of C5a in P-selectin expression and adhesiveness of neutrophils were similar to the effects of histamine and thrombin on endothelial cells. The adhesiveness of C5a-stimulated endothelium for neutrophils was blocked by anti-P-selectin, but not by antibodies to intercellular adhesion molecule 1, E-selectin, or CD18. A cell-based ELISA technique has confirmed upregulation of P-selectin in endothelial cells exposed to C5a. Binding of C5a to endothelial cells has been demonstrated, with molecules bound being approximately 10% of those binding to neutrophils. By a reverse transcriptase-PCR technique, endothelial cells have been shown to contain mRNA for the C5a receptor. These data suggest that C5a may be an important inflammatory mediator for the early adhesive interactions between neutrophils and endothelial cells in the acute inflammatory response.
New Cardiac Ablation Device Approved
Authors: Stuart L. Nightingale
Journal: JAMA (1994)

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
Tc-99m MDP Uptake Resulting From Acute Middle Cerebral Artery Territory Infarction
Authors: Gavin Christopher Mackie
Journal: Clinical Nuclear Medicine (2003)

Cerebral uptake of Tc-99m methylene diphosphonate is rare, occurring in less than 0.2% of patients undergoing bone scintigraphy. A case of acute cerebral infarction detected by Tc-99m methylene diphosphonate (MDP) scintigraphy is presented, demonstrating Tc-99m MDP uptake in the middle cerebral artery territory on delayed phase imaging. The findings were confirmed to be the result of cerebral infarction on computed tomography. This case highlights the role of extraosseous uptake of Tc-99m MDP in the detection of previously unrecognized pathology. Cerebral uptake of Tc-99m MDP is not specific for infarction and may occur in intracranial malignancy or with intracranial calcification from any cause.
Organ-Culture Methods in the Study of Gastrointestinal-Mucosal Function and Development
Authors: Howard L. Bleich, Emily S. Boro, Jerry S. Trier
Journal: New England Journal of Medicine (1976)

In vitro studies of mammalian gastrointestinal-mucosal function and metabolism are often limited by rapid autolysis of mucosal epithelial cells. Everted sacs1 or rings of intestine and fragments of gastric and colonic mucosa immersed in oxygenated buffer solutions2 are useful for short-term incubation, but morphologic examination shows epithelial-cell necrosis and cell degeneration if such incubations are prolonged for more than two to three hours.3 Similarly, most preparations of isolated epithelial-cell suspensions from the gastrointestinal tract remain viable for only a few hours. When grown in tissue cultures, these cells undergo rapid dedifferentiation,4 which is often accompanied by overgrowth of mesenchymal cells . . .
Learning to cope with violence in the workplace.
Authors: V Schnieden, J Maguire, A Bate
Journal: BMJ (1993)

on previously was taking both desmopressin and methylphenidate.2Desmopressin, imipramine, and methylphenidate are centrally acting drugs, which act as neurotransmitters.The antidiuretic action of desmopressin might possibly be augmented by imipramine and methylphenidate.We agree with Hamed and colleagues that parents should be warned of the dangers of excessive fluid intake when desmopressin is used.We suggest that current treatment with a centrally acting drug should be considered a relative contraindication to treatment with desmo- pressin.We also suggest that any patient who develops vomiting, headache, or nausea during treatment with desmopressin should stop taking the drug and see his or her doctor promptly.
CD5-negative chronic lymphocytic leukemia with indolent clinical course and autoimmune thrombocytopenia, successfully treated with rituximab
Authors: Masashi Okamoto, Sonoko Nakano, Kyoko Namura, Noriko Yamada, Ryo Uchida, Shin‐ichi Fuchida, Akira Okano, Naoya Ochiai, Chihiro Shimazaki
Journal: American Journal of Hematology (2004)

A 59-year-old male with lymphocytosis and thrombocytopenia was asymptomatic without lymphadenopathy or hepatosplenomegaly over 10 years. He was admitted to our hospital because his thrombocytopenia had worsened. The clonal lymphocytes appeared as regular small mature lymphocytes on blood films, and bone marrow biopsy showed diffuse infiltration of mature lymphocytes. However, megakaryocytes also presented. The immunophenotypic analysis by flow cytometry revealed that the lymphocytes were positive for CD19, CD20, CD22, and surface membrane immunoglobulin (SmIg) M and D-lambda and were negative for CD5, CD10, CD11c, CD23, and other lineage markers. Expression levels of CD20 and SmIg were strong. The markers were consistent with CD5- CLL with autoimmune thrombocytopenia. He received rituximab, and a rapid decrease of lymphocytes with concomitant increase of platelets was observed. A few cases of CD5- CLL with a stable clinical course have been reported, thought to be B lymphocytosis of undetermined significance (MLUS). This is the first report of CD5- CLL with indolent clinical course associated with autoimmune thrombocytopenia, successfully treated with rituximab.
ANTIBIOTICS IN DISEASES OF THE BILIARY TRACT
Authors: Jerry Zaslow
Journal: JAMA (1953)

As new antibiotic or chemotherapeutic agents have been introduced into the therapeutic armamentarium, many of them have been used in the treatment of biliary tract disease. Improvement observed following the use of these drugs has often been attributed to them. This has been due to the fact that each of these drugs, in the course of pharmacological observations, has been shown to be excreted into the normal biliary tract of lower animals or humans. Until I began to study the excretion and concentration of antibiotic and chemotherapeutic agents in the abnormal human biliary tract, no one had approached the problem from that aspect. Since that time I have studied the excretion and concentration of the sulfonamides, penicillin, streptomycin, aureomycin, and, more recently, oxytetracycline (Terramycin). As a result of these investigations it became apparent that the excretion and concentration in the abnormal biliary tract was entirely different from that in the
Olfactory detection of human bladder cancer by dogs: Another cancer detected by “pet scan”
Authors: James S Welsh
Journal: BMJ (2004)

Olfactory detection of human bladder cancer by dogs Cause or association?Editor-The study by Willis et al, testing whether dogs can detect signs of bladder cancer in urine, may be the occasion for an amusing cover for the BMJ but this should not be an excuse for relaxing intellectual rigor when assessing the experiment. 1 Neither the authors nor the commentator point out that the study design is unable to distinguish cause from association-a basic logical error.The dogs may be detecting "tumour related volatile compounds" or they may be detecting a substance in the urine that is associated with an increased risk of cancer.The most obvious candidate would be from cigarette smoking, which would be rather unoriginal, but it could also be other as yet unidentified substances.Furthermore, while the dogs may only be 41% accurate at detecting urine from people already diagnosed with cancer, the results would also be consistent with a higher accuracy for detecting patients at risk of cancer.The authors should follow up their interesting preliminary study rigorously and the BMJ should stick to the Christmas edition for letting down its usual standards of review.
GMC considers widening number of cases it will divert from formal hearings
Authors: C. Dyer
Journal: BMJ (2009)

Many more doctors who are investigated by the UK’s General Medical Council for allegedly providing substandard care could be allowed to avoid a public hearing by giving undertakings that they will retrain or practise under supervision.

The regulatory body is to consult on widening the range of cases in which doctors are offered “consensual disposal” at the investigation stage, as an alternative to sending the case to be heard by a fitness to practise panel.

The option, originally limited to cases of ill health …
Abstract 5007: WT1 promotes tumor growth and vascularization by regulating matrix metalloproteinase 9 in Ewing's sarcoma xenografts
Authors: Varalakshmi Katuri, Hans- Joerg Hammers, Stephanie Gerber, Xiaofei Qiu, Elizabeth Montgomery, David M. Loeb
Journal: Cancer Research (2011)

Abstract WT1, a zinc-finger transcription factor, is expressed in tumors of varied origins including sarcomas. High level WT1 expression often correlates with poor patient survival. The role of WT1 in sarcoma biology and the mechanism by which high WT1 expression confers a poor prognosis are both unclear. The aim of this study is to investigate the effect of WT1 expression on sarcoma growth and angiogenesis. We transfected the WT1-null Ewing's sarcoma cell line SK-ES-1 with one of two major WT1 isoforms, and used shRNA to silence WT1 expression in the WT1-positive Ewing's sarcoma cell line MHH-ES. Cells were injected into the flanks of immune deficient mice and tumor growth was monitored. Tumors arising fromWT1-expressing SK-ES-1 cells grew faster than control, while tumors arising from WT1-silenced MHH-ES cells grew more slowly than control. Because our laboratory and others have shown that WT1 regulates VEGF expression, we evaluated tumor vascularity using the endothelial cell marker CD31 and the pericyte marker αSMA. In xenografted SK-ES-1 cells, quantification of CD31 positive area in WT1 expressing tumors showed 60 -70 % more compared to the controls. In contrast, CD31 expression is abolished in tumors arising from WT1-silenced MHH-ES cells. To investigate the mechanism by which WT1 affects tumor growth and vascularity, we performed a gene expression profiling in SK-ES-1 cells expressing different isoforms of WT1. We identified a number of genes up- or downregulated by WT1, including matrix metalloproteinase-9 (MMP9). Luciferase reporter assays showed that WT1 can upregulate MMP9 promoter activity in transiently transfected NIH3T3 cells. Also, immunohistochemical analysis showed increased MMP9 expression in WT1-expressing tumors. Finally, imunohistochemical analysis of primary Ewing's sarcoma samples showed correlated expression of WT1, VEGF, and MMP9. Taken together, our data suggest that WT1 promotes tumor growth and angiogenesis, perhaps via upregulation of MMP9. Increased tumor angiogenesis may lead to more aggressive tumors and a worse outcome for patients, explaining the effect of WT1 on prognosis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5007. doi:10.1158/1538-7445.AM2011-5007
Abstract 2968: TH17 cells in early pancreatic tumorigenesis
Authors: Florencia McAllister, Jennifer M. Bailey, Jeffrey Roeser, Danielle T. Blake, Elizabeth C. Wick, Cynthia L. Sears, Elizabeth M. Jaffee, Jay K. Kolls, Charles G. Drake, Drew M. Pardoll, Steven D. Leach
Journal: Cancer Research (2012)

Abstract Activating Kras mutations have been detected in 30% of pancreatic intraepithelial neoplasias (PanIN), increasing to 100% in advanced pancreatic ductal adenocarcinoma (PDAC). Chronic pancreatitis is a risk factor for PDAC and cigarette smoking, the most important single risk factor for PDAC, has been recently associated with chronic pancreatic inflammation. The central hypothesis guiding our work is that inflammatory cells recruited to the pancreas in response to chronic injury can interact with epithelial cells harboring activated KrasG12D, affecting the progression of PanIN lesions. Further understanding of this interaction would be fundamental to generate effective chemopreventive strategies in high risk populations. To test this hypothesis, we have used the Mist1:CreERT2; LSL-KrasG12D mice in which the LSL KrasG12D allele is activated specifically in the acinar compartment of adult mice, leading to the rapid formation of PanIN with a classic “ductal” phenotype. We have established a model of chronic inflammation- induced pancreatic tumorigenesis that results in significant acceleration in the initiation and progression of PanIN lesions at 4 weeks after the activation of Kras. We have found that TH17 cells, a subtype of CD4+ T-helper cells known to play an active role in other models of inflammation- induced tumorigenesis, are rapidly recruited to the pancreas after Kras activation and are further increased in the presence of concomitant chronic pancreatic inflammation induced by cerulein injections. The differentiation of CD4+T cells into TH17 requires IL-6 and TGF-B, and both factors are increased in the pancreatic tumor microenvironment. Finally, Stat3, a key transcription factor that determines the differentiation of Th17 lineage, is activated in cells infiltrating early PanIN lesions. We are currently evaluating both genetic ablation of TH17 cells and neutralizing antibodies against IL-17 as novel therapeutics strategies in murine PanIN. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2968. doi:1538-7445.AM2012-2968
A glycine zipper motif mediates the formation of toxic β-amyloid oligomers in vitro and in vivo
Authors: Virginia Fonte, Vishantie Dostal, Christine M Roberts, Patrick Gonzales, Pascale Lacor, Jordi Magrane, Natalie Dingwell, Emily Y Fan, Michael A Silverman, Gretchen H Stein, Christopher D Link
Journal: Molecular Neurodegeneration (2011)

The β-amyloid peptide (Aβ) contains a Gly-XXX-Gly-XXX-Gly motif in its C-terminal region that has been proposed to form a "glycine zipper" that drives the formation of toxic Aβ oligomers. We have tested this hypothesis by examining the toxicity of Aβ variants containing substitutions in this motif using a neuronal cell line, primary neurons, and a transgenic C. elegans model.We found that a Gly37Leu substitution dramatically reduced Aβ toxicity in all models tested, as measured by cell dysfunction, cell death, synaptic alteration, or tau phosphorylation. We also demonstrated in multiple models that Aβ Gly37Leu is actually anti-toxic, thereby supporting the hypothesis that interference with glycine zipper formation blocks assembly of toxic Aβ oligomers. To test this model rigorously, we engineered second site substitutions in Aβ predicted by the glycine zipper model to compensate for the Gly37Leu substitution and expressed these in C. elegans. We show that these second site substitutions restore in vivo Aβtoxicity, further supporting the glycine zipper model.Our structure/function studies support the view that the glycine zipper motif present in the C-terminal portion of Aβ plays an important role in the formation of toxic Aβ oligomers. Compounds designed to interfere specifically with formation of the glycine zipper could have therapeutic potential.
An Address ON MINING ACCIDENTS: WITH AN ACCOUNT OF THE USE OF OXYGEN IN A COALPIT ACCIDENT: Delivered to the Stirling Branch of the British Medical Association
Authors: J. Robertson
Journal: BMJ (1909)

X ACH' 20, T90 bacilli is bt once diminished, the lactic acid bacilli being easily demonstrable in the dejeCta for some -time Afterwards.We find, however, that with suitable doses of enriched cultures accustomed to live under anaerobic' conditions, and administered in a specific acid medium, there is no difficulty in demonstrating the presence of the bacili in 'the stool passed the following morning.It is not an easy matter to recognize the various lactic acid bacilli in the faeces, and only when we adopted the acid "gastric" medium referred to did we find the pro- cedure at all simplified.By this means, however, the recognition is neither difficult nor tardy, and the prac- titioner is assured of a practical demonstration of the object he aims at.These lactic acid bacilli are not in their natural habitat when transferred to the colon, and it ia-curious that their life in the intestine is abotit the same as it is in artificial media-namely, about five to seven days.This seems to be the period when another dose is indicated.The fact suggests that we must not expect these bacilli to become accHmatized to the intestine easily, and must regard them rather as temporary interlopers, our object being to allow the normal flora to regain their sway as soonas the objectionable putrefactive anaerobes are ovetcome.Pa'sage of Lactic Acid Ferment8 through the Alimentary Canal.Tablets from the various preparations were taken by the mouth.When the organism appeared in the faeces the ingestion was stopped, and the faeces examined daily until the lactic acid ferment could no longer be *olated.TABLE XI.
Prognostic Influence of Mutational Status in Resected Non-Small Cell Lung Cancer: the KRAS G12V Worse Value
Authors: S. Renaud, P.-E. Falcoz, M. Schaeffer, M. Beau-Faller, B. Romain, A. Olland, J. Reeb, N. Santelmo, G. Massard, A.-C. Voegeli
Journal: Annals of Oncology (2015)
The AMA and Torture
Authors: J. James Rohack
Journal: JAMA (1986)

<h3>To the Editor.—</h3> As a profession, medicine is dedicated to healing. It is natural for physicians to be concerned when medical skills are used in manners opposite to healing. We read with pleasure your editorial requesting the American Medical Association (AMA) House of Delegates to adopt a resolution reaffirming the stand against physician participation in torture.<sup>1</sup> Similar concern was expressed by Dr Louis Daily, a Houston ophthalmologist, at a winter meeting of the Harris County Medical Society. The result was adoption of a resolution at the Texas Medical Association House of Delegates meeting in Dallas in May 1986, which was forwarded to the AMA House of Delegates for consideration at the Annual Meeting. I had the privilege of testifying before Reference Committee H, representing Texas on Resolution 91. Your editorial provided further support for our resolution. The Reference Committee recommended adoption and the AMA House of Delegates concurred on
Catecholamine Release in Familial Dysautonomia
Authors: Alfred A. Smith, Joseph Dancis
Journal: New England Journal of Medicine (1967)

PROMINENT among the symptoms of familial dysautonomia are the manifestations of autonomic dysfunction.1 A disturbance in catecholamine metabolism has been documented by the demonstration of high homovanillic acid and low vanillyl-mandelic acid urinary excretion rates.2 This evidence of pressor catecholamine insufficiency correlates well with the postural hypotension that is consistently found in familial dysautonomia Infusions of relatively small amounts of norepinephrine produce hypertension and patchy erythema,3 suggesting heightened reactivity to sympathetic substances, rather than an excessive production of norepinephrine, as the cause of the clinical symptoms.The abnormality in catecholamine metabolism has now been further explored by measurement of the . . .