tbuckley/cabot-search huggingface dataset:
First Immunotoxin Therapy for Many Common Solid Tumors Enters Phase I Clinical Trial
Authors: Andrew A. Skolnick
Journal: JAMA (1993)

THE FIRST clinical trial of an immunotoxin that is genetically engineered to target a variety of common solid tumors is under way at the National Cancer Institute (NCI), Bethesda, Md. The phase I trial, which began in April, involves patients with breast or colon cancers that do not respond to conventional therapies. Ira Pastan, MD, chief of the NCI's Laboratory of Molecular Biology and coinventor of the immunotoxin, described the development of this new type of anticancer agent at a conference in Chicago, Ill. The conference, DNA: The Double Helix— Forty Years: Perspective and Prospective, was cosponsored by The New York (NY) Academy of Sciences, The University of Illinois at Chicago, and Green College, Oxford University, England. So far only seven of the 20 to 30 patients Pastan hopes to enroll in the trial have been treated with a protocol for determining the toxic effects of his experimental drug, B3-LysPE38.
HFE mutations and transferrin receptor polymorphism analysis in porphyria cutanea tarda: a prospective study of 36 cases from southern France
Authors: O. Dereure, P. Aguilar-Martinez, D. Bessis, P. Perney, C. Vallat, B. Guillot, F. Blanc, J-J. Guilhou
Journal: British Journal of Dermatology (2001)

Porphyria cutanea tarda (PCT) is associated in most cases with iron overload, which may participate in decreased activity of uroporphyrinogen decarboxylase in the liver. The aetiology of this iron overload remains unknown; however, it has been demonstrated that mutations of HFE, the genetic haemochromatosis gene, might be present in a significant proportion of Anglo-Saxon and Italian patients. Furthermore, transferrin receptor polymorphism may influence the affinity of this receptor to its ligand with a subsequent increase of cellular iron absorption and storage.To evaluate the incidence and spectrum of HFE mutations and the relative frequency of the two main alleles of transferrin receptor in patients with PCT originating from southern France, and to evaluate the relationship of these genetic data with iron status, and with hepatitis B and C and human immunodeficiency virus (HIV) infections.Thirty-six consecutive patients with either sporadic or familial PCT were prospectively included between 1997 and 2000. Search for the presence of the three main mutations of the HFE gene and identification of the transferrin receptor alleles were performed using polymerase chain reaction followed by enzymatic digestion. Iron parameters and viral status for hepatitis B and C viruses and HIV were determined.Seven patients (19%) showed heterozygous C282Y mutation, but no C282Y homozygote was present; five patients (14%) carried homozygous H63D mutation, while eight (22%) were heterozygous for this mutation. One patient was heterozygous for the S65C mutation (3%). Iron parameters demonstrated overload in all patients, without a clear difference between patients with and without deleterious mutations of the HFE gene. Infection by hepatitis C virus was documented in 20 patients (56%), and was significantly less frequent in patients with deleterious HFE mutations. The profile of transferrin receptor alleles in PCT patients did not show significant variation compared with the general population.This study confirms the high frequency of HFE mutations in patients with PCT and supports the hypothesis that HFE gene abnormalities might play a significant part in the PCT pathomechanism, probably through iron overload; by contrast, transferrin receptor polymorphisms do not appear to play a significant part in iron overload in PCT.
Sample Features Associated with Success Rates in Population-Based EGFR Mutation Testing
Authors: Carolyn J. Shiau, Jesse P. Babwah, Gilda da Cunha Santos, Jenna R. Sykes, Scott L. Boerner, William R. Geddie, Natasha B. Leighl, Cuihong Wei, Suzanne Kamel-Reid, David M. Hwang, Ming-Sound Tsao
Journal: Journal of Thoracic Oncology (2014)
Abstract 2343: A novel ERK inhibitor is active in models of acquired resistance to BRAF and MEK inhibitors.
Authors: Ahmed A. Samatar, Erick J. Morris, Sharda Jha, Restaino R. Clifford, Bart Luttrerbach, Marc Pelletier, Ulrike Philippar, Lata Jayaraman, Leigh Zawel, Steve Fawell, Gary Gilliland
Journal: Cancer Research (2013)

Abstract The high frequency of activating BRAFV600E mutations in melanoma (40-70%), thyroid (50%) and colorectal cancer (10%), or KRAS/NRAS mutations in melanoma (20%), pancreatic (90%), colorectal (50%) and non-small cell lung cancer (30%), provides strong rationale for targeting the MAPK pathway as a therapeutic strategy 1-6. Vemurafenib (PLX4032) and dabrafenib (GSK2118436), selective BRAF inhibitors, and trametinib (GSK1120212), an allosteric MEK inhibitor, have shown robust clinical efficacy in melanoma patients 7-10. However, the majority of responses are transient and cellular resistance is often associated with pathway reactivation involving the downstream extracellular-signal-regulated kinases 1 and 2 (ERK1/2) (reviewed in 11). We hypothesized that pathway blockade at ERK, the last signaling node prior to MAPK transcriptional programming, would not only be efficacious in MAPK-activated tumors but would also have utility in BRAF or MEK inhibitor resistant settings. We therefore sought to identify small molecule inhibitors of ERK. This report describes the identification and characterization of SCH772984, a potent and selective ATP competitive inhibitor of ERK1/2 which displays behaviors of both type I and type II kinase inhibitors. SCH772984 has nanomolar cellular potency on tumor cells with mutations in BRAF, NRAS, or KRAS and induces tumor regressions in xenograft models at tolerated doses. Importantly, SCH772984 effectively inhibited MAPK signaling and cell proliferation in BRAF or MEK inhibitor resistant models as well as in the context of BRAF/MEK combination resistance. Together these data support the clinical development of ERK inhibitors, not only in patients with MAPK activated tumors, but also in patients who have developed acquired resistance to BRAF or MEK inhibitors or resistance to the recently described combination of these agents. Citation Format: Ahmed A. Samatar, Erick J. Morris, Sharda Jha, Restaino R. Clifford, Bart Luttrerbach, Marc Pelletier, Ulrike Philippar, Lata Jayaraman, Leigh Zawel, Steve Fawell, Gary Gilliland. A novel ERK inhibitor is active in models of acquired resistance to BRAF and MEK inhibitors. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2343. doi:10.1158/1538-7445.AM2013-2343
Hypoactivity of the Hypothalamo-Pituitary-Adrenal Axis in Victims of Mobbing: Role of the Subjects&amp;rsquo; Temperament and Chronicity of the Work-Related Psychological Distress
Authors: Palmiero Monteleone, Giovanni Nolfe, Cristina Serritella, Valter Milano, Arcangelo Di Cerbo, Francesco Blasi, Claudio Petrella, Mario Maj
Journal: Psychotherapy and Psychosomatics (2009)
252. A Novel Approach of Gentamicin Therapy for Duchenne Muscular Dystrophy Using Hybrid Liposome and Establishment of a System To Identify the Patients Eligible for the Treatment
Authors: Shigemi Kimura, Kaori Ito, Shro Ozasa, Hiroe Kawano, Makoto Ikezawa, Makoto Matsukura, Ryuichi Ueoka, Yoko Matsumoto, Msafumi Matsuo, Yasuhiro Takeshima, Teruhisa Miike
Journal: Molecular Therapy (2005)

Aminoglycoside antibiotics have been found to suppress nonsense mutations located in the defective dystrophin gene in mdx mice, suggesting a possible treatment for Duchenne muscular dystrophy (DMD). However, the gentamicin therapy is hindered by several problems. First, a high dose of gentamicin, which is needed to induce a read-through of the nonsense mutations in DMD patients, can not be given because of oto- and nephrotoxicity. Even if this dose could be tolerated, this high concentration cannot be sustained due to the short half-life of gentamicin. Lastly, identifying patients that are applicable for this therapy is difficult because: 1) only 5 to 13% of DMD patients have nonsense mutations in the dystrophin gene, 2) it is challenging to find nonsense mutations in the gene because dystrophin cDNA is very long (14kb), and 3) the efficiency of aminoglycoside-induced read-through is dependent on the kind of nonsense mutation.
Treatment of oral lichen planus with topical pimecrolimus 1% cream
Authors: L. Esquivel-Pedraza, L. Fernandez-Cuevas, G. Ortiz-Pedroza, E. Reyes-Gutierrez, R. Orozco-Topete
Journal: British Journal of Dermatology (2004)

Journal Article Treatment of oral lichen planus with topical pimecrolimus 1% cream Get access L. Esquivel‐Pedraza, L. Esquivel‐Pedraza Departments of Dermatology and Pathology, Instituto Nacional de Ciencias Médicas y Nutrición 'Salvador Zubirán', Vasco de Quiroga 15, Tlalpan 14000, México, D.F., Mexico Search for other works by this author on: Oxford Academic Google Scholar L. Fernández‐Cuevas, L. Fernández‐Cuevas Dentistry School, Universidad Intercontinental, Insurgentes Sur 4303, Sta. Ursula Xitla, Tlalpan 14420 and Universidad Latinoamericana, Gabriel Mancera 1409, Del Valle 3100, México, D.F., Mexico E‐mail: lillyep@hotmail.com Search for other works by this author on: Oxford Academic Google Scholar G. Ortíz‐Pedroza, G. Ortíz‐Pedroza Departments of Dermatology and Pathology, Instituto Nacional de Ciencias Médicas y Nutrición 'Salvador Zubirán', Vasco de Quiroga 15, Tlalpan 14000, México, D.F., Mexico Search for other works by this author on: Oxford Academic Google Scholar E. Reyes‐Gutiérrez, E. Reyes‐Gutiérrez Departments of Dermatology and Pathology, Instituto Nacional de Ciencias Médicas y Nutrición 'Salvador Zubirán', Vasco de Quiroga 15, Tlalpan 14000, México, D.F., Mexico Search for other works by this author on: Oxford Academic Google Scholar R. Orozco‐Topete R. Orozco‐Topete Departments of Dermatology and Pathology, Instituto Nacional de Ciencias Médicas y Nutrición 'Salvador Zubirán', Vasco de Quiroga 15, Tlalpan 14000, México, D.F., Mexico Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 150, Issue 4, 1 April 2004, Pages 771–773, https://doi.org/10.1111/j.0007-0963.2004.05875.x Published: 01 April 2004
Health-Related Quality of Life in Patients with Advanced Nonsquamous Non–Small-Cell Lung Cancer Receiving Bevacizumab or Bevacizumab-Plus-Pemetrexed Maintenance Therapy in AVAPERL (MO22089)
Authors: Achim Rittmeyer, Vera Gorbunova, Anders Vikström, Arnaud Scherpereel, Joo-Hang Kim, Myung-Ju Ahn, Antonio Chella, Christos Chouaid, Alicyn K. Campbell, Fabrice Barlesi
Journal: Journal of Thoracic Oncology (2013)
A Potential Use of the National Death Index for Postmarketing Drug Surveillance
Authors: Stanley A. Edlavitch, Manning Feinleib, Charles Anello
Journal: JAMA (1985)

A particularly difficult problem for both the Food and Drug Administration and the pharmaceutical manufacturer is evaluation of the importance of spontaneous reports of suspected drug-associated fatalities. These reports are rare, and usually no accurate denominator data on drug use exist. This article proposes that the National Death Index be used to calculate mortality rates for selected drugs as part of the postmarketing surveillance efforts of the government and manufacturers. When hypotheses are generated from spontaneous reports and/or the mortality data, additional studies can be conducted on the cohorts that were identified for mortality follow-up.
Dame Janet's disappointments
Authors: Glyn Elwyn
Journal: BMJ (2006)

“ G ood riddance to blind faith in doctors,” was the opening line made by Dame Janet Smith at the “After Shipman” conference, held by the Royal Society of Medicine last week. The high court judge who chaired the Shipman Inquiry was reflecting on the manner in which the murders by the infamous general practitioner, and other more recent cases of medical misconduct, had broken the pillar of trust between the public and the profession. Her view was that blind faith should be replaced by transparent standards: doctors who fail against such measures “should be removed from practice”—reiterating the key argument she made in her final report on the inquiry.

> Strong leadership in the medical profession could do more 

Dame Janet then listed her disappointments, arguing that there had been little, if any, action taken by the government or the General Medical Council in response to her raft of recommendations. Death certification reforms have not been initiated. …
ATP antagonism of thrombin-induced endothelial barrier permeability
Authors: D GUNDUZ, F HIRCHE, F HARTEL, C RODEWALD, M SCHAFER, G PFITZER, H PIPER, T NOLL
Journal: Cardiovascular Research (2003)

Objectives: Thrombin induces endothelial barrier failure by activating the contractile machinery of endothelial cells. Contractile activation is due to an increase in myosin light chain (MLC) phosphorylation. Here, it was investigated whether stimulation of endothelial cells with ATP can interrupt this thrombin-induced pathomechanism. Methods: In cultured human umbilical vein endothelial cells, cytosolic calcium [Ca2+]i (Fura 2 method), phosphorylation of MLC, isometric tension and permeability for albumin were studied. Results: Thrombin (0.2 U/ml) increased [Ca2+]i from a basal level of 78±8 to 570±63 nM (mean±S.D., n = 5, P<0.05), MLC phosphorylation from 71±7 to 163±18%, isometric tension from 157±17 to 232±26 μN, and permeability from 2.8±0.4 to 11.6±1×10−6 cm/s. Co-presence of ATP (10 μM) and thrombin did not alter the [Ca2+]i rise, but reduced MLC phosphorylation to 59.8±10%, isometric tension to 174±14 μN, and permeability to 5.4±0.6×10−6 cm/s. The thrombin-induced rise in MLC phosphorylation was sensitive to reduction of [Ca2+]i It was accompanied by an increase in Rho activation, and was inhibited by Y-27632 (10 μM), a Rho-kinase blocker. The ATP-induced decrease in MLC phosphorylation was not sensitive to [Ca2+]i. It was not accompanied by changes in RhoA activation, and could not by suppressed by Y-27632. Conclusions: ATP antagonizes the Ca2+- and Rho-dependent effects of thrombin on MLC phosphorylation most likely by a Ca2+- and Rho-independent activation of MLC phosphatase. It thereby functionally antagonizes the thrombin-induced increase in monolayer tension and permeability.
Post-transplant lymphoproliferative disorders (PTLD) after liver transplantation (LT). Role of HCV infection
Authors: C. Hézode, C. Duvoux, G. Germanidis, F. Roudot-Thoraval, JM Métreau, A. Bastie, D. Cherqui, JM Pawlotsky, D Dhumeaux
Journal: Journal of Hepatology (1998)
Uganda saw prevalence of AIDS rise by a third from 2007 to 2013, report says
Authors: H. Wasswa
Journal: BMJ (2014)

The number of Ugandans living with HIV or AIDS is rising steadily, partly because people with the infection are living longer thanks to antiretroviral drugs and partly because of its continuing spread.

Between 2007 and 2012 the number increased from 1.2 million to 1.5 million, …
Wide QRS-Complex Tachycardia
Authors: Keith D. Wrenn
Journal: Annals of Internal Medicine (1989)

Letters and Corrections1 March 1989Wide QRS-Complex TachycardiaKeith D. Wrenn, MDKeith D. Wrenn, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-110-5-412_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editor:The article on wide QRS-complex tachycardia by Akhtar and colleagues (1) is a welcome treatise on the electrocardiographic diagnosis of this complex and often enigmatic arrhythmia. Although I agree with most of their conclusions, I must take issue with two points. First, that "ventricular tachycardia makes up an overwhelming majority of cases" is not definitively answered by a study made up of patients referred to cardiologists experienced in electrophysiologic evaluation. There is an inherent bias in this tertiary referral that cannot be easily explained away. Although this supposition may be correct, a large trial of consecutive patients...References1. Akhtar M, Shenasa M, Jazayeri M, Caceres J, and Tchou P. Wide QRS complex tachycardia: reappraisal of a common clinical problem. Ann Intern Med. 1988;109:905-12. LinkGoogle Scholar2. Wellens H. The wide QRS tachycardia [Editorial]. Ann Intern Med. 1986;104:879. LinkGoogle Scholar3. Lown B and de Silva R. Cardioversion and defibrillation. In: Hurst JW, Logue RB, Rackley CE, et al., eds. The Heart: Arteries and Veins. 6th ed. New York: McGraw-Hill Book Co.; 1986:1742-5. Google Scholar4. Steward R, Bardy G, and Greene H. Wide complex tachycardia: misdiagnosis and outcome after emergent therapy. Ann Intern Med. 1986;104:766-71 LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Keith D. Wrenn, MDAffiliations: Emory University School of Medicine Atlanta, GA 30303 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byWide Complex TachycardiaManagement strategies in wide QRS complex tachycardia 1 March 1989Volume 110, Issue 5 Page: 412-412 Keywords Arrhythmia Electrocardiography Electrophysiological techniques Tachycardia Ventricular tachycardia ePublished: 1 December 2008 Issue Published: 1 March 1989 PDF downloadLoading ...
Transient Left Ventricular Dilatation in the Absence of Epicardial Disease on Angiography
Authors: Kevin K.L. Choong, Paul A. Russell
Journal: Clinical Nuclear Medicine (2004)

A 58-year-old woman with a previous anterior myocardial infarction, recurrent chest pain, transient adenosine-induced left ventricular dilatation but no apparent epicardial disease on angiography is presented. Transient ischemic dilatation during myocardial perfusion imaging, and the reported causes of transient left ventricular dilatation in the absence of epicardial disease, are discussed.
Acute Pneumonia and Pneumothorax as a Complication of Transbronchial Biopsy
Authors: M. Muers, D. Lane
Journal: Endoscopy (1980)

This report describes the development of an acute pneumonia and a pneumothorax after transbronchial biopsy with a fiberoptic bronchoscope. The patient was elderly and had a chronic bronchopneumonia. The literature is reviewed and it is concluded that elderly patients with chronic pyogenic pulmonary infections may represent a high risk category for this investigation.
New agenda for general practice computing
Authors: M. Walker
Journal: BMJ (1990)

In the same publication we also reported the phenomenon of upward setting of the glucoregulatory centre in diabetes (as alluded to by Dr Ryder and colleagues).We showed that those diabetic subjects who retained adequate counterregulatory capacity did so at a significantly higher blood glucose concentration than did the normal group.Our data, however, do not confirm the suggestion of Dr Ryder and colleagues that recurrent hypoglycaemia may be the cause of the counter- regulatory failure.We studied both insulin dependent and non-insulin dependent diabetic subjects and found that the counterregulatory defect occurred in both types of diabetes.It is highly unlikely that recurrent hypoglycaemia occurred in the subject using only diet to control diabetes or the two subjects with tablet failure.Thus recurrent hypoglycaemia is probably not the sole cause of this abnormality.
Hyperinfection Syndrome with Strongyloides stercoralis
Authors: EZEQUIEL RIVERA
Journal: Annals of Internal Medicine (1970)

Infection with the parasitic nematode, Strongyloides stercoralis, can lead to death in patients with various clinical disorders. Alteration of the parasite—host relationship may lead to hyperinfection characterized by profound malabsorption, diarrhea, electrolyte imbalance, gram-negative or opportunistic fungal sepsis, coma, and death. During the last 3 years nine such patients were studied in the hematology section of a 300-bed university hospital. Eight patients died, four in spite of energetic treatment with thiabendazole. Since diagnosis of hyperinfection is often made only at autopsy, its presence should be suspected in hematologic patients and patients with diseases of altered immunity, such as leprosy and systemic lupus erythematosus. Since early diagnosis is essential to avoid fatalities, laboratory technicians and physicians dealing with such patients as well as with large population groups that harbor this parasite (for example, Puerto Ricans) should be alerted.
Regulation of medical research is hampering improvement in US health care, critics say
Authors: B. Roehr
Journal: BMJ (2009)

Regulations and practices in the United States designed to protect patients and their privacy are impeding medical research and in some instances making it prohibitively expensive, a leading medical society says. 

The rules are hindering improvements in care, says the Infectious Disease Society of America in an article in Clinical Infectious Diseases (2009;49:328-35, doi:10.1086/605454). The society is seeking to clarify and simplify the regulations while maintaining protection of patients.

A big obstacle, the society’s article says, is the Health Insurance Portability and Accountability Act, enacted in 1996 to protect patients in care, with a rolling series of implementation dates. But research carried out with informed consent is a very different situation from standard health care, said William Burman, director of the infectious disease clinic at Denver Public Health and head …
Bone Mineral Density and High-Trauma Fractures—Reply
Authors: Dawn C. Mackey
Journal: JAMA (2008)

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
ACUTE MYELOGENOUS LEUKAEMIA WITH C-MYC AMPLIFICATION AND DOUBLE MINUTE CHROMOSOMES
Authors: Kari Alitalo, Robert Winqvist, Jorma Keski-Oja, Mirja Ilvonen, Kalle Saksela, Riitta Alitalo, Marikki Laiho, Sakari Knuutila, Albert De La Chapelle
Journal: The Lancet (1985)
THE POTENTIAL OF EBCT FOR CORONARY ARTERY CALCIUM SCREENING TO EVALUATE FATTY LIVER: DALLAS HEART STUDY
Authors: Susan Matulevicius, Laura C. Huff, Colby R. Ayers, Roderick McColl, Lydia Sczcepaniak, Amit Khera, Ronald M. Peshock
Journal: Journal of the American College of Cardiology (2010)