tbuckley/cabot-search huggingface dataset:
Suppression of the Primary Rh Immune Response with Passive Rh IgG Immunoglobulin
Authors: Vincent J. Freda, John G. Gorman, William Pollack
Journal: New England Journal of Medicine (1967)

THAT passive immunity can block active immunity is an established concept dating from as early as 1909.1 The precise mechanism of the immunosuppressive action, however, is still not clearly understood, but it is now being intensely studied by many investigators.2 3 4 In 1960 we put this principle to use5 6 7 8 9 and initiated a program to determine whether initial immunization of Rh-negative mothers by Rh of fetal origin could be prevented by the passive administration of Rh antibody immediately after childbirth. At the same time, and quite independently, Finn and Clarke and their co-workers10 , 11 began similar experimental work. Our aims were as follows: . . .
THE EFFECT OF CERTAIN DRUGS UPON THE GALVANIC SKIN RESPONSE.
Authors: B. SHACKEL
Journal: British Journal of Dermatology (1958)

Journal Article THE EFFECT OF CERTAIN DRUGS UPON THE GALVANIC SKIN RESPONSE. Get access B. SHACKEL, M.A. B. SHACKEL, M.A. Psychological Research Laboratory, EMI Etectronics Ltd Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 70, Issue 5, 1 May 1958, Pages 155–165, https://doi.org/10.1111/j.1365-2133.1958.tb13310.x Published: 01 May 1958
Parliament prepares for a health audit
Authors: J. Warden
Journal: BMJ (1994)

For an administration that shies away from health legislation the British government is in the unlikely position of having to pilot three separate health bills through the new session of parliament (p 1389). Having previously thought themselves overexposed with one bill, ministers will now have to put their heads above the parapet three times: on health service restructuring, the performance of doctors, and supervision of mentally ill people in the community.

This all comes about because at a late stage the cabinet got cold feet about privatising the Royal Mail. The consequent gap in the Queen's speech prompted opposition assertions that after 15 years of office the Conservatives had finally run out of steam. That hit a sensitive nerve in Downing Street and the call went out for departments to come …
Preventive Health Care
Authors: Cecil G. Sheps
Journal: JAMA (1982)

The editor promises to deal chiefly with methods for the implementation of primary prevention, that is, general and specific measures to prevent the onset of disease. The book is intended for health practitioners in primary care clinics. There are 48 chapters on a vast range of subjects, some only three or four pages long, written by 30 authors (26 of whom are faculty members of one medical school), resulting in the unevenness of quality often characteristic of such ventures. Although there are a few good chapters, such as the ones on child health and prenatal care for the low-risk gravida, most are devoted to elementary, general descriptions of entities of disease or disability, with little, if any, specificity about measures of intervention for primary prevention. Despite the stated purpose of this collection of chapters, many focus heavily on secondary prevention—preventing the progression of a disease—and neglect primary prevention. The opening
Phase 1 Experience with an Anti-Glycotope Monoclonal Antibody, RAV12, in Recurrent Adenocarcinoma
Authors: Howard A. Burris, Lee S. Rosen, Caio M. Rocha-Lima, John Marshall, Suzanne Jones, Roger B. Cohen, Lori A. Kunkel, Deryk Loo, Jan Baughman, Stanford J. Stewart, Nancy Lewis
Journal: Clinical Cancer Research (2010)

RAV12 is a high affinity, internalizing, chimeric IgG1 monoclonal antibody that binds RAAG12, a novel primate-restricted N-linked carbohydrate epitope present on multiple cell surface proteins. RAAG12 is highly expressed on many adenocarcinomas, particularly those of gastrointestinal origin. A phase 1 dose-escalation safety and pharmacokinetics trial was conducted in patients with metastatic or recurrent adenocarcinomas.RAV12 was initially given i.v. weekly x4, then by fractionated dosing twice or thrice weekly. Thirty-three patients were treated in the dose escalation segment of the trial in the following cohorts: 0.3 mg/kg qw (6), 1.0 mg/kg qw (8), 1.5 mg/kg qw (7); and 0.5 mg/kg biw (3), 0.75 mg/kg biw (3), and 0.5 mg/kg tiw (6). Twenty patients were enrolled in a maximum tolerated dose cohort expansion at 0.75 mg/kg biw.Two clinical syndromes were associated with drug administration: abdominal cramping pain with diarrhea, and asymptomatic, self-limited increases of liver function tests. These effects were partially ameliorated with fractionated dosing. Pharmacokinetics was dose dependent. Maximum concentration was reduced, whereas area under the concentration versus time curve was maintained with fractionated dosing. One patient with colorectal cancer experienced a durable partial remission, with a time to progression (TTP) of >8 months. Three additional patients experienced a TTP of >4 months.RAV12 has activity in recurrent adenocarcinomas. However, the safety profile of the antibody seems to preclude the delivery of highly efficacious doses. Re-engineering the molecule to remove FcRn binding (while maintaining FcgammaR binding) and to humanize it may improve the toxicity profile and efficacy.
Peptidyl-prolyl isomerases: a full cast of critical actors in cardiovascular diseases
Authors: Gianluca Lorenzo Perrucci, Aoife Gowran, Marco Zanobini, Maurizio Colognesi Capogrossi, Giulio Pompilio, Patrizia Nigro
Journal: Cardiovascular Research (2015)

Peptidyl-prolyl cis-trans-isomerases are a highly conserved family of immunophilins. The three peptidyl-prolyl cis-trans-isomerase subfamilies are cyclophilins, FK-506-binding proteins, and parvulins. Peptidyl-prolyl cis-trans-isomerases are expressed in multiple human tissues and regulate different cellular functions, e.g. calcium handling, protein folding, and gene expression. Moreover, these subfamilies have been shown to be consistently involved in several cardiac and vascular diseases including heart failure, arrhythmias, vascular stenosis, endothelial dysfunction, atherosclerosis, and hypertension. This review provides a concise description of the peptidyl-prolyl cis-trans-isomerases and presents an incisive selection of studies focused on their relationship with cardiovascular diseases.
Antibodies to Yersinia enterocolitica in Thyroid Disease
Authors: Louis Shenkman, Edward J. Bottone
Journal: Annals of Internal Medicine (1976)

The prevalence of elevated antibody titers against Yersinia enterocolitica was studied in normal subjects, patients with a variety of nonthyroidal illnesses, and patients with thyroid disease. In contrast to the low prevalence of antibodies in controls (less than 8%), 48 of 67 patients (75%) with a variety of thyroid disorders had titers greater than 1:8. Antibodies were found in 24 of 36 patients with Graves' disease, five of six with autonomous adenoma, seven of seven with Hashimoto's thyroiditis, three of five with idiopathic primary hypothyroidism, four of 11 with nontoxic nodular goiter, and one of two with thyroid carcinoma. Antibodies to serotype 3 were the most prevalent, occurred in the highest titers, and were found particularly in patients with Graves' disease. These observations indicate that in spite of the infrequent occurrence of yersinia infection in the United States as compared with Scandinavia, patients with thyroid disorders have a higher prevalence of antibodies to Yersinia than normal subjects or patients with other disorders.
SECOND–GENERATION EVEROLIMUS–ELUTING STENTS VERSUS FIRST–GENERATION DRUG–ELUTING STENTS FOR PATIENTS TREATED FOR MULTIVESSEL DISEASE
Authors: Sa'ar Minha, Israel Barbash, Danny Dvir, Itsik Ben–Dor, Joshua Loh, Salem Badr, Lakshmana Pendyala, Hironori Kitabata, Lowell Satler, Augusto Pichard, William Suddath, Kenneth Kent, Rebecca Torguson, Ron Waksman
Journal: Journal of the American College of Cardiology (2013)
BRCA1 and BRCA2 Founder Mutations and the Risk of Colorectal Cancer
Authors: B. L. Niell, G. Rennert, J. D. Bonner, R. Almog, L. P. Tomsho, S. B. Gruber
Journal: JNCI Journal of the National Cancer Institute (2004)

Background: Mutations in BRCA1 and/or BRCA2 (BRCA1/2) profoundly increase the risks of breast and ovarian cancers, but it is unclear whether mutations in these genes increase the risk of colorectal cancer. We investigated BRCA1/2 founder mutations and a family history of breast cancer as potential risk factors for colorectal cancer. Methods: In the population-based Molecular Epidemiology of Colorectal Cancer study in northern Israel, 1422 case patients with incident colorectal cancer, diagnosed between March 31, 1998, and December 31, 2002, and 1566 control subjects without colorectal cancer were genotyped for the BRCA1 187delAG, BRCA1 5385insC, and BRCA2 6174delT founder mutations. Genotypes and interview data from all case patients and control subjects and from only those of Ashkenazi Jewish descent (1002 case patients and 1038 control subjects) were used to calculate odds ratios [ORs] from logistic regression. Results: Twenty-four (2.4%) case patients and 20 (1.9%) control subjects carried one of the three mutations (OR = 1.24, 95% confidence interval [CI] = 0.68 to 2.26). A family history of breast cancer in a female relative was not associated with an increased risk of colorectal cancer, even after adjustment for the presence of a BRCA founder mutation (OR = 1.03, 95% CI = 0.75 to 1.41). Conclusions: Although weak associations cannot be excluded, Ashkenazi BRCA founder mutations do not confer a strongly elevated risk of colorectal cancer. Similarly, a family history of breast cancer does not appear to be a strong risk factor for colorectal cancer in this population.
Abstract 4548: The role of GPR30/G-protein coupled estrogen receptor (GPER) in lung cancer development
Authors: Venkatakrishna R. Jala, Haribabu Bodduluri, Brandie Radde, Carolyn M. Klinge
Journal: Cancer Research (2011)

Abstract Lung cancer is currently the leading cause of cancer deaths both in men and women. Estrogens, including 17β-estradiol (E2), are known to promote various cancers including breast, endometrial, and ovarian cancers. Women are at higher risk for lung adenocarcinoma than men, implying a potential role for estrogens in lung cancer. E2 mediates its genomic effects through two well-characterized nuclear receptors, estrogen receptor α (ERα) and estrogen receptor β (ERβ), both of which are expressed in normal lung and lung adenocarcinomas. In addition to genomic estrogen action, i.e., transcriptional regulation of gene expression, estrogens activate rapid, non-genomic responses such as intracellular calcium release, cAMP production, MAPK and PI3K/AKT phosphorylation, and up regulation of c-fos transcription. These observations prompted a search for new estrogen receptors and culminated in the discovery of GPR30 (GPER) as a bona fide estrogen receptor that mediates some of the membrane actions of E2. GPR30 is a seven transmembrane G-protein coupled receptor (GPCR) unrelated to nuclear ERα and ERβ. Although GPR30 is expressed in healthy lung, its expression in lung tumors/lung cancer cell lines as well as its functional activities has not been investigated. In the current study, we investigated the expression of GPR30 in human and murine lung cancer cell lines and tumor tissues both at the transcript and protein levels. Our analyses demonstrated for the first time that GPR30 expression is significantly increased (2 to140 fold) in lung cancer cells lines (A549, H1435, H1395, H1944, H1792, H1793, H2073, H23, H1299, LLC) compared to immortalized normal human bronchioepithelial cells (HBEC3-ET, HBEC2-E, HBEC2-KT). The expression of GPR30 in lung tissue microarrays (LC242, LC1005 from USBiomax) containing 87 cases of lung cancer tissues along with normal and cancer adjacent tissues were analyzed by immunohistochemnistry (IHC). IHC scores confirm that GPR30 is significantly overexpressed in more than 80% of lung adenocarcinomas (p&amp;lt;0.0001), 75% of large cell carcinoma (p&amp;lt;0.0001) and 60% in squamous cell carcinoma (SCC) (p&amp;lt;0.0001). These observations suggest that E2, as well as other GPER ligands, signaling through GPR30 might play a critical role in lung carcinogenesis independent of the classical ERα and ERβ. Given the cross-talk between GPR30, ERα and epidermal growth factor receptor (EGFR) reported in other cell types, we suggest that blocking the signaling activities of GPR30, ERα, and EGFR may synergize to provide a better therapeutic option for treating lung cancer. 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 4548. doi:10.1158/1538-7445.AM2011-4548
The Financing of Biomedical Research
Authors: Donald L. Madison
Journal: JAMA (1990)

The story of how the National Institutes of Health extramural grant programs grew following World War II is familiar political lore. The best versions are Elizabeth Drew's 1967<i>Atlantic Monthly article</i>"The Health Syndicate: Washington's Noble Conspirators" and Stephen Strickland's book<i>Politics, Science and Dread Disease</i>(1972). In explaining the current status of biomedical research funding, Eli Ginzberg and Anna B. Dutka cover some of the same ground as Drew and Strickland, but, unlike these earlier accounts,<i>The Financing of Biomedical Research</i>is not narrative history. It is rather an analysis of the flow of money—the ups and downs and shifting channels. Yet, there is a story here, too. Between 1940 and 1987, national spending on biomedical research increased (in constant, uninflated dollars) by 4000%. Most of the new funds came from the federal government, which in 1940 had been responsible for only 7% of the spending on biomedical research
Review: Rifaximin is equally or more effective than other antibiotics and lactulose for hepatic encephalopathy
Authors: Joe Alcorn
Journal: Annals of Internal Medicine (2008)

ACP Journal ClubNovember 18, 2008Review: Rifaximin is equally or more effective than other antibiotics and lactulose for hepatic encephalopathyJoe Alcorn, MDJoe Alcorn, MDUniversity of New Mexico, Albuquerque, New Mexico, USA (J.A.)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-149-10-200811180-02011 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Source CitationLawrence KR, Klee JA. Rifaximin for the treatment of hepatic encephalopathy. Pharmacotherapy. 2008; 28:1019-32. https://pubmed.ncbi.nlm.nih.gov/18657018Clinical Impact RatingsGastroenterology: References1 Lizardi-Cervera J, Almeda P, Guevara L, Uribe M. Hepatic encephalopathy: a review. Ann Hepatol. 2003;2:122-30. [PMID: 15115963] Google Scholar2 Sanaka MR, Ong JP, Mullen KD. Challenges of designing hepatic encephalopathy treatment trials. Hepatology. 2003;38:527-8. [PMID: 12903650] Google Scholar3 Ruiz J, Mensa L, Pons MJ, Vila J, Gascon J. Development of Escherichia coli rifaximin-resistant mutants: frequency of selection and stability. J Antimicrob Chemother. 2008;61:1016-9. [PMID: 18325895] Google Scholar4 Huang E, Esrailian E, Spiegel BM. The cost-effectiveness and budget impact of competing therapies in hepatic encephalopathy—a decision analysis. Aliment Pharmacol Ther. 2007;26:1147-61. [PMID: 17894657] Google Scholar5 Wiest R, Garcia-Tsao G. Bacterial translocation (BT) in cirrhosis. Hepatology. 2005;41:422-33. [PMID: 15723320] Google Scholar Author, Article, and Disclosure InformationAffiliations: University of New Mexico, Albuquerque, New Mexico, USA (J.A.) PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics November 18, 2008Volume 149, Issue 10Page: JC5-11KeywordsAdverse reactionsAmmoniaAntibioticsAntimicrobial resistanceAntimicrobialsBloodBrain diseasesCirrhosisClinical trialsCohort studiesDatabasesDrug therapyElectroencephalographyMorbidityNeomycinsNeurophysiologyPatientsSafetySigns and symptoms ePublished: 10 March 2020 Issue Published: November 18, 2008 Copyright & PermissionsCopyright © 2008 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Correction of Advertising Mischief
Authors: Harry V. Unfug
Journal: JAMA (1974)

<h3>To the Editor.—</h3> I would like to pass along to fellow members two workable suggestions for decreasing unwanted medical bulk advertising. Simply write a big "NO" on the address label and return in the postage reply envelope most of what these mailings include. They may get the hint. Or, write to: Direct Mail/Marketing Association, Inc., 6 East 43rd St, New York, NY 10017, to request their Mail Preference Form, on which you can indicate the type of mailings you wish to receive or not receive. I have calculated that the doctors in America receive 50,000,000 pounds of unnecessary papyrodiarrhea annually.
Does baseline qrs‐width predict long‐term benefit of resynchronization therapy for congestive heart failure?
Authors: S. Sack, A. Auricchio, P. Bakker, J. Vogt, M. Kloss, H. Kirkels, P. Potty, R. Salo, A. Doelger, P. Cuesta
Journal: European Journal of Heart Failure (2000)
Salvage of the Ischemic Limb
Authors: Victor M. Bernhard
Journal: JAMA (1968)

Limb salvage was achieved in 30 (77%) of 39 patients subjected to bypass surgery for end stage ischemia. Pressure gradients were reduced to zero after aortofemoral bypass; however, a small residual gradient was usually present after femoral-popliteal vein graft. Arterial flows were markedly increased at all levels following bypass. There was no difference in postoperative flow between patients whose limbs were salvaged and those with lesser degrees of ischemia. Average flow per extremity was 270 ml/min after aorto-iliac bypass and 100 ml/min after femoral-popliteal bypass. Local intra-arterial infection of papaverine hydrochloride increased flow to 170 ml/min following femoral-popliteal bypass. Ultimate flow potential of the limb may be estimated by this test. Failure to increase flow with papaverine suggests technical error.
Sustained appetite improvement in malnourished dialysis patients by daily ghrelin treatment
Authors: Damien R. Ashby, Heather E. Ford, Katie J. Wynne, Alison M. Wren, Kevin G. Murphy, Mark Busbridge, Edwina A. Brown, David H. Taube, Mohammad A. Ghatei, Frederick W.K. Tam, Stephen R. Bloom, Peter Choi
Journal: Kidney International (2009)
Delay in diagnosis of breast cancer after screening is associated with bigger tumours
Authors: D. Spurgeon
Journal: BMJ (2002)

Delays of more than 20 weeks between an abnormal breast cancer screen and diagnosis of the disease in asymptomatic women are associated with increased size of tumours and increased risk of metastases of the lymph nodes, says a study in the American Cancer Society's journal Cancer (2002;52:2143-50). [ed. note, added 24 May 2002: the correct citation is Cancer (2002:94:2143-50)]

A group of investigators, led by Dr Ivo Olivotto of British Columbia's screening mammography programme, analysed data in the Canadian breast …
No Salt Substitute
Authors: Marshall Morgan
Journal: JAMA (1971)

To the Editor. —  Shapiro et al recently found that hyperkalemia secondary to potassium chloride therapy was a common cause of fatal drug reactions in a large group of medical inpatients (216:467-472, 1971).  Inpatients placed on salt-restricted diets are sometimes given potassium chloride as a salt substitute without the physician's knowledge. In two major teaching hospitals, I have seen this practice cause severe hyperkalemia in patients with oliguric renal failure.  As a result, I routinely specify No Salt Substitute when writing diet orders for such patients.
Abstract 2927: Breast tumor kinase (Brk/PTK6) mediates hypoxia/HIF-1α-associated breast cancer progression.
Authors: Tarah Regan Anderson, Gregory Hubbard, Andrea R. Daniel, Danielle Peacock, Roland H. Wenger, Alexandra Schörg, David Hoogewijs, George Vande Woude, Tiffany N. Seagroves, Carol A. Lange
Journal: Cancer Research (2013)

Abstract Triple negative (basal type) breast cancers are more aggressive and difficult to treat relative to HER2/ER/PR positive (luminal type) breast cancers; these tumors frequently express abundant Met receptors and contain high constitutive levels of hypoxia inducible factor alpha (HIF-1α), a principal mediator of cellular stress that predicts cancer relapse and increased risk of metastasis. Breast tumor kinase (Brk/PTK6; Sik in mice) is a soluble tyrosine kinase that is not found in normal breast tissue, but is aberrantly expressed in up to 86% of all breast cancers. We recently showed that Brk is a critical downstream effector of Met signaling and required for HGF-induced cell migration. Herein, we show that Brk and HIF-1α are co-expressed in human triple negative cell lines and tumors. Brk mRNA and protein levels are strongly upregulated during conditions that induce cellular stress in vitro, including low glucose, H2O2, and hypoxia. Chromatin-immunoprecipitation (ChIP) assays revealed that Brk is a direct early transcriptional target of HIF-1α; HIF knockdown demonstrated that Brk expression is dependent upon both HIF-1α and HIF-2α. Notably, Brk expression rescued the growth of MDA-MB-231 xenografts knocked-down for both HIF1α and HIF2α in vivo. Finally, we crossed WAP-Brk (FVB) transgenic mice into the MMTV-METmut model (FVB mice engineered to express MMTV-driven constitutively active mutant Met receptors); the addition of the human wt Brk transgene decreased survival in this model. Notably, mouse mammary tumors that arose in MMTV-METmut mice expressed abundant Sik, the mouse homolog of Brk; high Sik expression conferred markedly decreased latency to tumor formation independently of the presence of the Brk transgene. These results identify HIF-1α as a novel regulator of Brk mRNA expression and suggest that Brk is a key mediator of HIF-1α-induced breast cancer progression. Targeting Brk expression or activity (downstream of the HGF/Met receptor signaling pathway) may provide an effective means to block the progression of deadly triple-negative breast cancers. Citation Format: Tarah Regan Anderson, Gregory Hubbard, Andrea R. Daniel, Danielle Peacock, Roland H. Wenger, Alexandra Schörg, David Hoogewijs, George Vande Woude, Tiffany N. Seagroves, Carol A. Lange. Breast tumor kinase (Brk/PTK6) mediates hypoxia/HIF-1α-associated breast cancer progression. [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 2927. doi:10.1158/1538-7445.AM2013-2927
Polyethylene glycol reduces the inflammatory injury due to cold ischemia/reperfusion in autotransplanted pig kidneys1Drs. Hauet and Goujon contributed equally to this work.
Authors: Thierry Hauet, Jean Michel Goujon, Hervé Baumert, Isabelle Petit, Michel Carretier, Michel Eugene, Alain Vandewalle
Journal: Kidney International (2002)