tbuckley/cabot-search huggingface dataset:
Tumor Necrosis Factor α and Regulation of Adipose Tissue
Authors: Erik Arner, Mikael Rydén, Peter Arner
Journal: New England Journal of Medicine (2010)

To the Editor: In patients with obesity, adipose tissue is characterized by low-grade inflammation and increased secretion of several cytokines.1 Tumor necrosis factor α (TNF-α) and interleukin-6 may be most pernicious, since they alter adipose-tissue function, influence adipogenesis, and are involved in the metabolic complications of obesity.1 However, adipose inflammatory cytokines may be not only culprits but also important players in normal adipose-tissue function, since inflammation may be essential for sensing nutritional needs and maintaining homeostasis in adipose tissue.2 If this is true, there should be a relationship between cytokine release and characteristics of adipose tissue in lean, healthy subjects. . . .
c-Jun N-terminal kinase-dependent mechanisms in respiratory disease
Authors: B. L. Bennett
Journal: European Respiratory Journal (2006)

Respiratory diseases pose a multifaceted dilemma. Although the symptoms and pathology are obvious and provide multiple opportunities for therapeutic investigation, at the same time, the molecular complexities and prioritisation are overwhelming. Even within a disease such as asthma, the number of inducers, cell types, secondary mediators, chemical changes, immune responses and tissue modifications is remarkable. One means of therapeutically targeting this complexity is to identify individual factors responsible for regulating multiple disease processes. The mitogen-activated protein kinase family integrates multiple diverse stimuli, and, in turn, initiates a cell response by phosphorylating and thereby modulating the activity of many target proteins. The c-Jun N-terminal kinase is a critical regulator of pro-inflammatory genes, tissue remodelling and apoptosis, and, therefore, represents an attractive target for novel therapies. Pre-clinical and clinical investigation into the efficacy of c-Jun N-terminal kinase inhibitors has been ongoing since the late 1990s. Over the course of this work, hypotheses have shifted as to the role of c-Jun N-terminal kinase in the many processes that promote allergic, inflammatory, obstructive and fibrotic diseases of the lung. Inhibition of c-Jun N-terminal kinase may indeed provide a means of suppressing more pathological mechanisms in respiratory disease than first suspected.
Rapidly Progressive Glomerulonephritis in Behçet's Syndrome
Authors: Douglas M. Landwehr
Journal: JAMA (1980)

Rapidly progressive glomerulonephritis developed in a patient with Behçet's syndrome while he was being treated with transfer factor. The therapy did not prevent development of this disease and thus cannot be recommended in patients who have Behçet's syndrome with renal involvement. (<i>JAMA</i>244:1709-1711, 1980)
The Elvis of pharmaceuticals
Authors: C. Elliott
Journal: BMJ (1996)

Since its humble beginning as a mere antidepressant in the late 1980s, Prozac has toured the celebrity circuit. It has appeared on morning talk shows, featured on the covers of international news magazines, spawned several pharmaceutical imitators, and with books such as Listening to Prozac, Talking Back to Prozac, and Prozac Nation almost singlehandedly supported a cottage publishing industry. Prozac is no longer just a drug, it's an American cultural icon travelling a path from innovation via celebrity to cliche. It's the Elvis Presley of the pharmaceutical world. With Brain Candy, Prozac makes its Hollywood debut, and what it lacks in star power it more than makes up in bad taste.

Brain Candy is …
Abstract 1052: <i>In vitro</i> mechanism of action of AZD5363, a novel AKT inhibitor, in breast and prostate cancer cell lines
Authors: Hannah Greenwood, Claire Crafter, Barry Davies, Sabina Cosulich
Journal: Cancer Research (2011)

Abstract AKT (protein kinase B) is a key regulator of the phosphoinositide-3-kinase signaling pathway and plays a key role in mediating signals for cell growth, survival and differentiation. This pathway is among the most commonly de-regulated pathways in human cancer and represents a key target for therapeutic intervention. Here, we describe the in-vitro mechanism of action of AZD5363, a potent small molecule inhibitor of AKT1, AKT2 and AKT3. We show that treatment of breast and prostate cancer cell lines with AZD5363 leads to inhibition of phosphorylation of a number of AKT substrates including PRAS40, GSK-3β and the downstream marker, P70S6K. In the BT474c cell line, &amp;gt;90% inhibition of phosphorylation of PRAS40 was observed at 1uM and this effect was sustained for 24 hours. Inhibition of phosphorylation of 4E-BP1, a key regulator of protein translation, was also observed when treating cells with AZD5363. We demonstrate that inhibition of phosphorylation of 4EBP1 (Thr37/46) is associated with an induction of 4E-BP1 binding to the eIF4E-mRNA CAP complex within 1 hour of dosing with AZD5363, consistent with inhibition of CAP-dependent protein translation. Analysis of phenotypic endpoints indicates that AZD5363 is a potent inhibitor of proliferation in the majority of breast and prostate cell lines studied. In addition, in a subset of cell lines, treatment with AZD5363 was shown to induce a cytotoxic phenotype measured by a Sytox Green endpoint. In the BT474c cell line, 1uM AZD5363 inhibited phosphorylation of 4E-BP1 by 50% at 24 hours and induced 11% apoptosis at 72 hours. This data demonstrates that AZD5363 has profound effects on downstream effectors of the PI3K/AKT pathway consistent with that of an Akt inhibitor which results in an anti-proliferative, and in some cases cytotoxic, profile in breast and prostate cell lines. AZD5363 is currently in Phase I clinical trials. 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 1052. doi:10.1158/1538-7445.AM2011-1052
Quo Vadis Stare Decisis — Or the Death of Precedent Torts
Authors: William J. Curran
Journal: New England Journal of Medicine (1970)

MOST physicians do not understand the law of torts; or at least they do not want to understand it. This is the law under which persons can sue for money, even large amounts of money, because a personal wrong (that is, a tort) is committed against them by another. Such suits can include claims for money even where no property is taken or damaged and where no financial loss has occurred due to medical bills or loss of wages and so forth. Physicians, at least in the past, seem to have come from sterner stock. They believe that life contains . . .
Inflammatory biomarkers predict relapse in IBD
Authors: P Hanaway
Journal: Gut (2005)

After reading the paper presented by Costa et al ( Gut 2005; 54 :364–8) and the additional commentary by Pardi and Sandborn ( Gut 2005; 54 :321–2), we would like to underscore the potential importance of biomarkers to assess intestinal inflammation and we would like to add a clarification on the faecal calprotectin assay.

We agree with Pardi and Sandborn that other serological markers have not demonstrated clinical utility as predictors or monitoring tools of inflammatory bowel disease (IBD) activity.1 Studies are emerging to support the sensitivity and clinical utility of more selective and specific non-invasive markers of intestinal inflammation, such as faecal calprotectin.2,3 As we deepen our understanding of the molecular basis of IBD, we may find that the degree of inflammation and its role in recurrence differs between Crohn’s disease and ulcerative colitis. This is an important question raised in both articles.

When comparing the Costa study with the earlier …
An economic analysis of interventions for diabetes.
Authors: D C Klonoff, D M Schwartz
Journal: Diabetes Care (2000)

The objective of this article is to stratify interventions for diabetes according to their economic impact. We conducted a review of the literature to select articles that performed a cost-benefit analysis for 17 widely practiced interventions for diabetes. A scale for categorizing interventions according to their economic impact was defined. The 17 interventions were classified as follows: 1) clearly cost-saving, 2) clearly cost-effective, 3) possibly cost-effective, 4) non-cost-effective, or 5) unclear. Clearly cost-saving interventions included eye care and pre-conception care. Clearly cost-effective interventions included nephropathy prevention in type 1 diabetes and improved glycemic control. Possibly cost-effective interventions included nephropathy prevention in type 2 diabetes and self-management training. Non-cost-effective interventions were not identified. Interventions with unclear economic impact included case management, medical nutrition therapy, self-monitoring of blood glucose, foot care, blood pressure control, blood lipid control, smoking cessation, exercise, weight loss, HbA1c measurement, influenza vaccination, and pneumococcus vaccination. Widely practiced interventions for patients with diabetes can be clearly cost-saving and clearly cost-effective. These practices are attractive from both a medical and an economic perspective.
The Year 2000
Authors: J. Tauber
Journal: JAMA (1965)

<h3>To the Editor:—</h3> It was most interesting to read "In the Year 2000" ( MEDICAL NEWS,<i>JAMA</i><b>191</b>, Jan 4, 1965, adv p 31). I believe the legal problems will be enormously complex in the era of organ transplants. Transplantation of an animal head has been successful in at least one case, according to reports I have read. If such a procedure will be feasible any time in the future in human surgery, we shall face extra-ordinarily new medicolegal problems, regarding identity, family relationships, property ownership, etc. Whose identity will such a person have? The identity of the ex-proprietor of the head, or of the ex-proprietor of the body? To which family will he belong? If the one ex-proprietor was a licensed surgeon, the other one a licensed attorney, which license will the composite person have? Which property, bank account, and debt will be his? From which line will he inherit,
The U.K. Prospective Diabetes Study: A review
Authors: Robert C Turner
Journal: Diabetes Care (1998)

The objective of the U.K. Prospective Diabetes Study (UKPDS), initiated in 1977, was set up to determine whether improved blood glucose control in people with type 2 diabetes will prevent the complications of diabetes. The UKPDS was also designed to determine whether there are differences between conventional policy (diet therapy) and three different regimens of intensive treatment policy, based on sulfonylurea, metformin, or insulin. Interim efficacy analyses revealed that the intensive policies with sulfonylurea, insulin, and metformin were equally effective in reducing fasting plasma glucose concentrations. However, glucose and HbA1c measurements steadily increased with time, reflecting ongoing deterioration of β-cell function. Cardiovascular disease was the major cause of complications, and the risk factors included raised LDL cholesterol concentrations, low HDL cholesterol concentrations, elevated blood pressure, elevated HbA1c concentrations, and smoking. A final study report was issued in September 1998, when the median duration of therapy was 11 years.
Romania's policy of emptying its orphanages raises controversy
Authors: Grainger Laffan
Journal: BMJ (2005)

Romania claims to have removed one of the main obstacles to its entry to the European Union in 2007 after closing down a large number of its huge children's homes without resorting to overseas adoptions.

Its policy of returning abandoned youngsters to their natural families has meant that dozens of the state run institutions have closed their doors, and Romania is pledging to continue the programme, despite pressure from countries such as Israel and the United States that wanted overseas adoptions to be restarted.

The country's problems with large numbers of unwanted children began when the then dictator Nicolae Ceaucescu decided to increase the country's population. He banned sex education, contraception, and abortion and offered financial incentives to parents to produce large …
The Thyroid and Glucose Intolerance in Uremia
Authors: Sergio De Marchi, Emanuela Cecchin, Maurizio Borean
Journal: Annals of Internal Medicine (1983)

Letters and Corrections1 December 1983The Thyroid and Glucose Intolerance in UremiaSERGIO DE MARCHI, M.D., EMANUELA CECCHIN, M.D., MAURIZIO BOREAN, B.D.SERGIO DE MARCHI, M.D.Search for more papers by this author, EMANUELA CECCHIN, M.D.Search for more papers by this author, MAURIZIO BOREAN, B.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-99-6-883_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: We read with interest the recent report by the UCLA conference on thyroid function in nonthyroidal illness (1). Thyroid status in patients with chronic renal failure has been extensively investigated, but the long-term effect of dialysis therapy is not well understood. Early studies reported that thyroid hormone concentrations are below the normal range in about one third of uremic patients, triiodothyronine (T3) being especially lowered (2). The low T3 level has been considered to be a result of a decrease of peripheral tissue conversion of thyroxine (T4) to T3, which could be due either to a shift...References1. CHOPRA I, HERSHMAN J, PARDRIDGE W, and NICOLOFF J. Thyroid function in nonthyroidal illness. Ann Intern Med. 1983;98:946-57. LinkGoogle Scholar2. RAMIREZ G, O'NEIL W, JUBIZ W, and BLOOMER H. Thyroid disfunction in uremia: evidence for thyroidal and hypophyseal abnormalities. Ann Intern Med. 1976;84:672-6. LinkGoogle Scholar3. KOSOWICZ J, MALCZEWSKA B, and CZEKALSKI S. Serum reverse triiodothyronine in chronic renal failure. Nephron. 1980;26:85-9. CrossrefMedlineGoogle Scholar4. DE FRONZO R and ALVESTRAND A. Glucose intolerance in uremia: site and mechanism. Am J Clin Nutr. 1980;33:1438-45. CrossrefMedlineGoogle Scholar5. KABADY U, PREMACHANDRA B, and MAAYAN M. LOW serum T3 and raised reverse T3 in diabetes mellitus: normalization on improvement in hyperglycemia. Acta Diabet Lat. 1982;19:233-42. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: SERGIO DE MARCHI, M.D.; EMANUELA CECCHIN, M.D.; MAURIZIO BOREAN, B.D. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 December 1983Volume 99, Issue 6Page: 883-884KeywordsAttentionGlucose intoleranceMedical dialysisRenal failureThyroidThyroid hormonesThyroxineTriiodothyronine ePublished: 1 December 2008 Issue Published: 1 December 1983 PDF downloadLoading ...
Like Drug Names
Authors: BENJAMIN TEPLITSKY
Journal: Annals of Internal Medicine (1974)

Comments1 January 1974Like Drug NamesBENJAMIN TEPLITSKY, R.PH.BENJAMIN TEPLITSKY, R.PH.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-80-1-120_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: I have compiled a list of drugs whose names look alike or sound alike. When a pharmacist takes a prescription over the telephone or attempts to decipher a physician's handwriting, a drug product not intended by the prescriber might be dispensed. Such an error might be the result of sound-alike or look-alike drug names. Below is a partial list of such drug names, with striking similarities. Physicians are urged to exercise great care when writing or telephoning prescriptions.Psychiatric DrugsAtarax-EnaraxAventyl-BentylDoriden-LoridineDoriden-DoxidanElavil-AldorilEthinamate-EthionamideEthinamate-EthamideEtrafon-MetretonHaldol-HalodrinHaldol-HaldroneMarplan-MarplexMebaral-MedrolMebaral-MellarilMeprobamate-MeperganMeprobamate-MeperidineMetrazol-MintezolNembutal-Myambutol... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: BENJAMIN TEPLITSKY, R.PH. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 January 1974Volume 80, Issue 1Page: 120-120KeywordsDrugsExercisePharmacists ePublished: 1 December 2008 Issue Published: 1 January 1974 PDF downloadLoading ...
Abstract 1426: Cyclooxygenase-2 (COX-2) utilizes Jun N-terminal kinases to induce invasion but not tamoxifen resistance in MCF-7 breast cancer cells
Authors: Vianey Gonzalez-Villasana, Rene Nieves-Alicea, Vanity McMurtry, Armando Huaringa, Ann-Marie Simeone, Yolanda Gutierrez-Puente, Gabriel Lopez-Berestein, Ana M. Tari
Journal: Cancer Research (2011)

Abstract Elevated Cyclooxygenase-2 (COX-2) expression in breast tumors had been associated with a lower survival rate in patients with Estrogen Receptor α (ERα)-positive tumors. We propose that COX-2 reduces survival rate in breast cancer patients with ERα-positive tumors because COX-2 decreases tamoxifen sensitivity and increases invasive activity of breast cancer cells. We demonstrated that transfection of the COX-2 gene in the tamoxifen-sensitive, ERα-positive MCF-7 breast cancer cell line decreased the cells’ sensitivity to tamoxifen by about 5-fold, and increased their invasive activity by about 3-fold. Furthermore, we demonstrated that COX-2 utilizes PGE2 to activate Protein Kinase C (PKC) to induce these tumorigeneic effects. However, which downstream factors are recruited by the COX-2/PGE2/PKC pathway to induce tamoxifen resistance and breast cancer cell invasion are not known. Here we report that COX-2 increases the phosphorylation of Jun N-terminal kinase (JNK), but not that of extracellular signal regulated kinases (ERK1,2), p38 mitogen activated protein kinase, or Akt. Inhibition of JNK by a chemical inhibitor or siRNA led to decreased COX-2-mediated invasion. Yet, JNK inhibition did not affect COX-2-mediated tamoxifen resistance. We propose that JNK is a promising target to block invasion in patients whose tumors are ERα-positive and present high levels of COX-2. 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 1426. doi:10.1158/1538-7445.AM2011-1426
THE SWINE LUNGWORM AS A RESERVOIR AND INTERMEDIATE HOST FOR SWINE INFLUENZA VIRUS
Authors: Richard E. Shope
Journal: The Journal of Experimental Medicine (1941)

Multiple intramuscular injections of H. influenzae suis were found to precipitate swine influenza virus infections in a group of apparently normal swine. The most likely explanation of the phenomenon seemed to be that the animals, though healthy and susceptible, harbored the virus in some unknown manner. The factors possibly determining the phenomenon were explored experimentally but without success.
Abstract LB-246: Epithelial-mesenchymal transition (EMT) does not necessarily decrease the sensitivity of cancer cells to chemotherapeutic agents
Authors: Roman Mezencev, Neda Jabbari, John F. McDonald
Journal: Cancer Research (2012)

Abstract Epithelial to mesenchymal transition (EMT) has been recently associated with metastatic competence and therapy resistance of cancer cells and the need for development of EMT-targeted therapies has been emphasized. In this report we address the differential responses of breast cancer cell lines with epithelial and mesenchymal phenotypes to anticancer agents using pharmacoinformatics and experimental approaches. First, we identified breast cancer cell lines with epithelial-like and mesenchymal-like phenotypes among the National Cancer Institute (NCI) panel of 60 cell lines and analyzed their differential responses to 10,081 anticancer agents. Second, we evaluated chemotherapeutic response of a mesenchymal-like isogenic breast cancer cell line (MCF-7-Snail) stably transfected to express the EMT-inducing Snail transcription factor and its epithelial-like precursor cell line transfected with the control plasmid (MCF-7-neo). The results of both approaches are inconsistent with the claim that mesenchymal-like cancer cells are generally more resistant to anticancer agents. We found that most of the 10,081 agents examined did not display significantly different potencies between epithelial-like and mesenchymal-like cells. Of the 10,081 anti-cancer agents examined, only 78 displayed consistent differences in effect between epithelial-like and mesenchymal-like cells and all of these agents displayed a more potent effect against mesenchymal-like cell lines. MCF-7-Snail cells were found to be more sensitive to the cytotoxic effects of doxorubicin, 5-FU and methotrexate, while MCF-7-neo cells were more sensitive to gemcitabine and docetaxel and both of these isogenic cell lines were equally responsive to mitomycin C and vincristine. The relatively lower sensitivity of MCF-Snail cells to docetaxel and gemcitabine can be explained by their overexpression of TUBB4 and RRM1, respectively, as demonstrated by gene expression analysis (U133 Plus 2.0 Affymetrix microarrays). In contrast, the higher sensitivity of MCF-7-Snail cells to 5-FU may be due to the down-regulation of the DPYD gene in these cells. Compared to isogenic epithelial cells, MCF-7-Snail cells display down-regulation of the anti-apoptotic genes XIAP, BCL2L1 and NAIP. Collectively, our results indicate that EMT per se does not generally result in a greater resistance of cancer cells to chemotherapeutic agents, but it may, in some instances, result in increased sensitivity of cancer cells to specific chemotherapeutic agents. 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 LB-246. doi:1538-7445.AM2012-LB-246