tbuckley/cabot-search huggingface dataset:
Alternative Medicine — The Risks of Untested and Unregulated Remedies
Authors: Marcia Angell, Jerome P. Kassirer
Journal: New England Journal of Medicine (1998)

What is there about alternative medicine that sets it apart from ordinary medicine? The term refers to a remarkably heterogeneous group of theories and practices — as disparate as homeopathy, therapeutic touch, imagery, and herbal medicine. What unites them? Eisenberg et al. defined alternative medicine (now often called complementary medicine) as “medical interventions not taught widely at U.S. medical schools or generally available at U.S. hospitals.”1 That is not a very satisfactory definition, especially since many alternative remedies have recently found their way into the medical mainstream. Medical schools teach alternative medicine, hospitals and health maintenance organizations offer it,2 and . . .
Intra-ampullary protruding mass: unusual presentation of mucinous carcinoma of the pancreas
Authors: E. Lee, K. Joo, J. Cha, H. Shin, S. Jung, J. Lee, G. Kim
Journal: Endoscopy (2009)

A 71-year-old man was referred to our hospital with chronic alcoholic pancreatitis. He had a history of daily intake of alcohol and intermittent abdominal pain over the past 15 years. The biochemical tests were normal except for a mild increase in the gamma glutamyl transpeptidase level. Cancer antigen (CA) 19–9 was 118.1 U/mL (normal value < 27 U/mL). Abdominal computed tomography scan showed an enlarged pancreatic head with calcifications, a marked dilated upstream pancreatic duct, and parenchymal atrophy ([Fig. 1 a] and [Fig. 1 b]).
THE EFFECT OF 2-MERCAPTOETHANOL ON MURINE MIXED LYMPHOCYTE CULTURES
Authors: Michael J. Bevan, Ruth Epstein, Melvin Cohn
Journal: The Journal of Experimental Medicine (1974)

Mouse spleen cells which have been depleted of adherent cells do not respond to allogeneic lymphocytes in vitro. Their cytotoxic response can be restored by inclusion of mercaptoethanol in the medium. Mercaptoethanol is shown to have a stimulatory effect also on the response of normal (unseparated) spleen cells to alloantigens. The enhancement of the DNA-synthetic and cytotoxic response is similar, varying from 3.5-15-fold. Cytotoxic cells also appear in unmixed lymphocyte cultures in the presence of mercaptoethanol and fetal calf serum. The specificity of these background cytotoxic cells is not known.
Ten-year survival of second kidney transplants: Impact of immunologic factors and renal function at 12months
Authors: Stéphanie Coupel, Magali Giral-Classe, Georges Karam, Jean-François Morcet, Jacques Dantal, Diego Cantarovich, Gilles Blancho, Jean-Denis Bignon, Pascal Daguin, Jean-Paul Soulillou, Maryvonne Hourmant
Journal: Kidney International (2003)
Effect of Switching Antithrombin Agents for Primary Angioplasty in Acute Myocardial Infarction
Authors: George D. Dangas, Roxana Mehran, Eugenia Nikolsky, Bimmer E. Claessen, Alexandra J. Lansky, Bruce R. Brodie, Bernhard Witzenbichler, Giulio Guagliumi, Jan Z. Peruga, Dariusz Dudek, Martin Möckel, Adriano Caixeta, Helen Parise, Harvey White, Gregg W. Stone
Journal: Journal of the American College of Cardiology (2011)
Ethical problems in respiratory care: the role of the law
Authors: M A Branthwaite
Journal: Thorax (2001)

It is customary—albeit perhaps simplistic—to identify four ethical principles as the basis for good medical practice.1 These are beneficence, non-maleficence, respect for autonomy, and justice, primarily distributive justice. The challenge for the practising clinician is to determine a proper course of action when these principles conflict, particularly when the individual, social, or financial consequences of new and perhaps promising treatments are known incompletely. Decisions taken in good faith are now often subject to public comment or criticism, and the National Health Service and other legislation add further constraints by introducing new rights or prescriptive guidelines without necessarily identifying the resources to fulfil these obligations. Many of these concerns have been part and parcel of medical practice for centuries, but it is only recently that the aura of the always wise and caring practitioner has been challenged by an increasingly assertive and vociferous public, ready to seek legal redress for perceived or actual wrongs. There is, of course, no sound reason why judicial decisions are any more cogent on matters of ethical principle than those of the medical profession, but society has created a legal system to regulate the conduct of its members and empowers the judiciary to resolve conflict. Any consideration of the moral basis of medical practice must therefore also take account of judicial determination of those questions of principle which have reached the courts. Examples of ethical conflict spawned by lung disease are considered here in the light of decisions made by the English courts.

The surgical management of lung cancer is a good example of potential conflict between beneficence and non-maleficence. Surgery is painful and entails risk. Is this “maleficence” warranted by the anticipated “beneficence” of disease alleviated or even cured? The practitioner develops a trained enthusiasm to advocate treatment aimed at prolonging life but does …
RIGHT VENTRICLE LONGITUDINAL 2-D STRAIN REDUCTION AS A RESULT OF INTENSIVE TRAINING IN THE GROUP OF YOUNG, HIGH ENDURANCE ATHLETES
Authors: Marcin Konopka, Wojciech Krol, Andrzej Klusiewicz, Krystyna Burkhard, Jolanta Chwalbinska, Andrzej Pokrywka, Miroslaw Dluzniewski, Wojciech Braksator
Journal: Journal of the American College of Cardiology (2014)
Abstract C04: HGFL promotes the development and progression mammary tumors and represents an attractive therapeutic target
Authors: Nancy M. Benight, Purnima Wagh, Susan E. Waltz
Journal: Cancer Research (2013)

Abstract A standard therapy for breast cancer is the use of receptor tyrosine kinase (RTK) inhibitors. RTKs efficiently target multiple receptors, including the Ron transmembrane receptor, whose activation leads to increased survival, migration, and angiogenesis through signaling pathways such as PI3K/Akt and NF-κB. Ron overexpression is correlated with increased metastasis and poor outcomes in patients. The only ligand for Ron is hepatocyte growth factor-like protein (HGFL), which is an endocrine factor secreted into the circulation from the liver. Published reports demonstrated that ectopic overexpression of HGFL in cancer cells leads to increased metastasis. However, no studies have examined the role of endogenous HGFL in Ron activation during tumor development and metastasis. We sought to test the hypothesis that HGFL is required for Ron receptor activation and mammary tumorigenesis. We utilized mice with mammary-specific Ron overexpression (MMTV-Ron), which develop mammary tumors with 100% incidence. MMTV-Ron mice were crossed to HGFL deficient (HGFL-/-) mice to generate MMTV-Ron X HGFL-/- mice. We compared mammary hyperplasia and tumor latency in MMTV-Ron mice with and without HGFL serially at 2.5, 4, 6, 8 and 10 months. Additional mice were followed to established tumor kinetics and growth and to examine metastatic dissemination. MMTV-Ron X HGFL-/- mice displayed decreased mammary hyperplasia and a significant delay in the time to tumor formation compared to control mice. Kinase assays show that Ron activation is reduced in mice with HGFL loss. Tumor cell proliferation was different between the groups while markers of apoptosis (TUNEL IHC and cleaved caspase 3 expression) were significantly increased in MMTV-Ron X HGFL-/- mice compared to controls. Western blot analysis of tumor lysates showed diminished activation of NF-κB signaling associated with HGFL loss. In conclusion, our data show that HGFL promotes the development of mammary hyperplasia and mammary tumor formation by enhancing tumor cell survival, Ron activation and NF-κB signaling. These data suggest that HGFL represents an excellent target for inhibiting Ron mediated tumor growth in human disease. Citation Format: Nancy M. Benight, Purnima Wagh, Susan E. Waltz. HGFL promotes the development and progression mammary tumors and represents an attractive therapeutic target. [abstract]. In: Proceedings of the Third AACR International Conference on Frontiers in Basic Cancer Research; Sep 18-22, 2013; National Harbor, MD. Philadelphia (PA): AACR; Cancer Res 2013;73(19 Suppl):Abstract nr C04.
P4-02-05: The Regulation of Artemin Signalling by IGF-1 in Mammary Carcinoma Cells.
Authors: C Yip, D Liu, PE Lobie, JK Perry
Journal: Cancer Research (2011)

Abstract Artemin is a neurotrophic signalling factor which belongs to the glial-derived neurotrophic factor (GDNF) family of ligands. Artemin acts as a survival, proliferation and migration factor for a number of neurological cell types, by signalling through the RET (rearranged during transfection) receptor and, in most cases, the GDNF receptor (GFR)-a3 co-receptor. Recently, a number of published studies have implicated Artemin as a potential oncogene in several cell types, including mammary carcinoma cells. Other studies further indicate that Artemin may influence cancer progression and tamoxifen resistance in some breast cancers. Available clinical data has demonstrated that increased Artemin expression is correlated with decreased overall patient survival in breast cancer patients and a poor outcome in tamoxifen treated breast cancer patients. Here we investigate interaction between the Artemin and the insulin-like growth factor-1 (IGF-1) signal transduction pathways. Using mammary carcinoma cell lines, we demonstrate that IGF-1 treatment increases the endogenous expression of both Artemin and its endogenous receptors, RET and GFRa3. Semi-quantitative RT-PCR assays demonstrated that IGF-1 stimulated mRNA expression of Artemin as well as RET and GFRa3 in wild-type MCF-7 and ZR-75-1 cells in a time-dependent and dose-dependent manner. The same effect was not observed in wild-type T47D cells where IGF-1 did not increase Artemin mRNA expression. We also demonstrated that forced expression of Artemin in MCF-7 cells consistently enhanced the response of these cells to IGF-1 in a number of cell function assays. Forced expression of Artemin significantly enhanced IGF-1-mediated stimulation of total cell number in MCF-7 cells. Consistent with this, Artemin enhanced IGF-1-mediated stimulation of S-phase entry and cell survival. In a soft agar assay, forced expression of Artemin also enhanced IGF-1-mediated stimulation of colony formation. Conversely, depletion of Artemin expression using siRNA abrogated the response to IGF-1 stimulation in MCF-7 cells. Artemin depletion significantly decreased IGF-1-stimulated increase in total cell number by decreasing IGF-1-stimulated cell proliferation and protection from apoptotic cell death. In addition, forced expression of Artemin in MCF-7 cells reduced cell sensitivity to the IGF-1 receptor small molecule inhibitor, AG1024. In conclusion, we have demonstrated that IGF-1 increases Artemin mRNA and protein expression in the breast cancer cell lines MCF-7 and ZR-75-1 and have identified potential cross-talk between the Artemin and IGF-1 signalling pathways in MCF-7 cells. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P4-02-05.
Intestinal microbiota metabolism of l-carnitine, a nutrient in red meat, promotes atherosclerosis
Authors: Robert A Koeth, Zeneng Wang, Bruce S Levison, Jennifer A Buffa, Elin Org, Brendan T Sheehy, Earl B Britt, Xiaoming Fu, Yuping Wu, Lin Li, Jonathan D Smith, Joseph A DiDonato, Jun Chen, Hongzhe Li, Gary D Wu, James D Lewis, Manya Warrier, J Mark Brown, Ronald M Krauss, W H Wilson Tang, Frederic D Bushman, Aldons J Lusis, Stanley L Hazen
Journal: Nature Medicine (2013)
Computers in Medicine
Authors: John R. Kernodle
Journal: JAMA (1972)

Although the computer is not new to medicine, its growing popularity within the medical community at large certainly is. Currently, computer technology is being developed and applied to the health industry at an unprecedented rate, and health-related computer technology has become a popular topic at major medical conferences and symposia. A number of professional organizations, some of international dimensions, have been formed to further the use of computer technology within the health complex. In addition, the potential commercial value of computer technology has been recognized by many organizations eager to provide services to the health industry. Perhaps the most common tasks to which computers have been applied to date in the health field are billing and accounting, particularly for ambulatory patients. At present, for example, a variety of computer-oriented billing and associated practice-management systems are used at the office level of care. Some immediate advantages in the use of these
Caffeine Dependence Syndrome
Authors: Eric C. Strain
Journal: JAMA (1994)

The extent to which daily caffeine use is associated with a substance dependence syndrome similar to that associated with other psychoactive drugs is unknown. The purpose of this study was to assess volunteers who reported problems with their use of caffeine for evidence suggesting a diagnosis of caffeine dependence based on the generic criteria for substance dependence from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV).Case-series evaluations.An academic research center.Self-identified adults who believed they were psychologically or physically dependent on caffeine.Diagnoses made by a psychiatrist using a structured clinical interview that included a section on caffeine dependence based on genetic criteria for DSM-IV substance dependence.Double-blind caffeine-withdrawal evaluation.Ninety-nine subjects were screened for the study, and 16 were identified as having a diagnosis of caffeine dependence. Median daily caffeine intake was 357 mg, and 19% of subjects consumed less than the national (US) daily average of caffeine. Criteria used for making diagnoses (and rates of their prevalence) were as follows: withdrawal (94%), use continued despite knowledge of a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by caffeine use (94%), persistent desire or unsuccessful efforts to cut down or control use (81%), and tolerance (75%). Eleven subjects underwent the double-blind caffeine-withdrawal evaluation portion of the study, and nine (82%) of the 11 showed objective evidence of caffeine withdrawal, including eight of 11 with functional impairment.These results, together with other experimental evidence, suggest that caffeine exhibits the features of a typical psychoactive substance of dependence. It is valuable to recognize caffeine dependence as a clinical syndrome, since some people feel compelled to continue caffeine use despite desires and recommendations to the contrary.
Abstract 3805: Novel chemosensitive single-nucleotide polymorphism markers to targeted regimens in metastatic colorectal cancer
Authors: Jin Cheon Kim, Seon Young Kim, Dong Hyung Cho, Ye Jin Ha, Eun Young Choi, Chan Wook Kim, Seon Ae Roh, Tae Won Kim, Hyoung Seok Ju, Yong Sung Kim
Journal: Cancer Research (2011)

Abstract Purpose: Methods for predicting individual responsiveness to targeted chemotherapy are urgently needed, considering the frequent resistance and extremely high cost of such therapies. Experimental Design: A chemosensitive single-nucleotide polymorphism (SNP) discovery schema is presented that utilizes genome-wide SNP screening with a human SNP array, an in vitro chemosensitivity assay in 118 colorectal cancers, clinical association analysis in 98 patients who had received metastatic chemotherapy, and biological utility assessment using cell viability assays of transfected colorectal cancer (CRC) cells. Results: Eleven SNPs related to bevacizumab and cetuximab sensitivity were initially chosen during screening. Response rates and survival periods revealed that patients carrying specific alleles of the SNPs ANXA11 rs1049550, LINS1 rs11247226, or ITGA3 rs2230392 were chemosensitive to bevacizumab regimens, and patients with DFNB31 rs2274159, LIFR rs3729740, or ISX rs361863 were chemosensitive to cetuximab regimens. Cytotoxicity analyses using MTT and caspase-3 assays showed that all RKO and HCT116 CRC clones transfected with the reference alleles of LIFR rs3729740 and ISX rs361863 (G and C, respectively) were more sensitive to cetuximab regimens than those transfected with the substitution alleles. Conclusions: Chemosensitive SNP markers were identified using a novel three-step process. The chemosensitive markers LIFR rs3729740 and ISX rs361863 will hopefully predict responsive patients to cetuximab regimens, although further validation is needed in large cohorts. 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 3805. doi:10.1158/1538-7445.AM2011-3805
Irbesartan and Lipoic Acid Improve Endothelial Function and Reduce Markers of Inflammation in the Metabolic Syndrome
Authors: Srikanth Sola, Muhammad Q.S. Mir, Faiz A. Cheema, Nadya Khan-Merchant, Rekha G. Menon, Sampath Parthasarathy, Bobby V. Khan
Journal: Circulation (2005)

Background— The metabolic syndrome is associated with increased angiotensin II activity, induction of a proinflammatory and oxidative state, and endothelial dysfunction. We evaluated the ability of irbesartan, an angiotensin receptor blocker, and lipoic acid, an antioxidant, to affect endothelial function and inflammation in patients with the metabolic syndrome. Methods and Results— We randomized 58 subjects with the metabolic syndrome in a double-blinded manner to irbesartan 150 mg/d (n=14), lipoic acid 300 mg/d (n=15), both irbesartan and lipoic acid (n=15), or matching placebo (n=14) for 4 weeks. Endothelium-dependent and -independent flow-mediated vasodilation was determined under standard conditions. Plasma levels of interleukin-6, plasminogen activator-1, and 8-isoprostane were measured. After 4 weeks of therapy, endothelium-dependent flow-mediated vasodilation of the brachial artery was increased by 67%, 44%, and 75% in the irbesartan, lipoic acid, and irbesartan plus lipoic acid groups, respectively, compared with the placebo group. Treatment with irbesartan and/or lipoic acid was associated with statistically significant reductions in plasma levels of interleukin-6 and plasminogen activator-1. In addition, treatment with irbesartan or irbesartan plus lipoic acid decreased 8-isoprostane levels. No significant changes in blood pressure were noted in any of the study groups. Conclusions— Administration of irbesartan and/or lipoic acid to patients with the metabolic syndrome improves endothelial function and reduces proinflammatory markers, factors that are implicated in the pathogenesis of atherosclerosis.
AIDS and Testing for AIDS
Authors: Michael Kanter
Journal: JAMA (1986)

To the Editor.—  In the recent article, Status Report on the Acquired Immunodeficiency Syndrome, the Council on Scientific Affairs 1 calculated that testing blood components for human T-cell lymphotropic virus type III (HTLV-III) using Abbott Laboratories' enzyme-linked immunosorbent assay kit would result in 20,000 positive results annually. This calculation assumed there are 20 million blood donors annually and a prevalence rate of HTLV-III antibody in the general population of 0.1%. Unfortunately, the number of donors (D) multiplied by the prevalence of the antibody (P) equals the number of persons with HTLV-III antibody, not the number of positive test results, as these authors concluded. The number of positive results in fact is the sum of the number of true-positives plus the number of false-positives.  Standard probability theory 2 shows that true-positive equals D × P × sensitivity and false-positive equals D(1—P)(1—specificity). Thus, the expected number of positive results equals D × P
Hepatotoxicity After Methoxyflurane Administration
Authors: Neil C. Klein
Journal: JAMA (1966)

METHOXYFLURANE (Penthrane) is a shortchain halogenated ether which was developed as a general anesthetic by Van Poznak and Artusio<sup>1</sup>and has been in clinical use since 1959. Although chemically an ether, this compound has organic chloride and fluoride substituents similar to that of halothane. In view of this structural similarity it might be expected that increasing use of methoxyflurane will be associated with rare reports of drug-induced hepatic injury. To our knowledge, this is the first nonfatal case of suspected methoxyflurane hepatotoxicity with documented hepatocellular necrosis. <h3>Report of a Case</h3> In June 1965, a 58-year-old Negro woman (NYH 159-803) was seen in the outpatient department complaining of a persistent vaginal discharge. A friable lesion, which on biopsy proved to be a squamous-cell carcinoma was noted in the vaginal vault. She was admitted for treatment in July 1965. She had suffered from attacks of acute pelvic inflammatory disease in 1939 and 1946 with episodic, recurrent lower abdominal pain. A hysterectomy and bilateral salpingo-oophorectomy was performed in 1953.
Abstract 5639: hsa-miR-200a regulates VEGF-C to induce epithelial-mesenchymal transition in sorafenib resistance hepatocellular carcinoma cells.
Authors: Jean Chiou, Jen-Liang Su, Michael Hsiao
Journal: Cancer Research (2013)

Abstract Hepatocellular carcinoma (HCC) is one of the most common potentially lethal human malignancies worldwide. Although treatment and perioperative management have evolved in recent years with dramatic advances in diagnostic techniques, operative methods, and combined chemoradiotherapy, the prognosis of patients with liver cancer remains dissolve. Sorafenib, a multikinase inhibitor targeting angiogenesis of hepatocellular carcinoma (HCC), demonstrated survival benefits in recent clinical trials. However, disease stabilization with sorafenib lasts a few months, possibly due to the development of resistance. It has been reported that Vascular endothelial growth factor (VEGF)-C signaling through VEGFR-3 (VEGFR-3) mediates leukemic cell proliferation, survival, and resistance to chemotherapy. In this study, we will elucidated the molecular mechanisms of VEGF-C with sorafenib-resistance in hepatocellular carcinoma. Our results showed that recombinant VEGF-C protein protected Huh-7/WT cell from sorafenib treatment. Knockdown of VEGF-C in Huh7/SR (sorafenib-resistance) cells decreased the cell survival in sorafenib treatment. The sorafenib-resistant cells changed their appearance from epithelial type to mesenchymal type compared to control. In Affymetrix microarray and microRNA microarray assays, we also found significant differences between Huh7/WT and Huh7/SR cell lines. hsa-miR-200a was found down-regulated in Huh7/SR cells which was found to be associated with epithelial-mesenchymal transition (EMT). Overexpression of hsa-miR-200a was found to regulate VEGF-C to alter EMT status in Sorafenib-resistance HCC. In conclusion, EMT may induce VEGF-C and downstream signaling pathways which resulted in sorafenib-resistance in HCC and hsa-miR-200a was found to be playing an important role in this process. Citation Format: Jean Chiou, Jen-Liang Su, Michael Hsiao. hsa-miR-200a regulates VEGF-C to induce epithelial-mesenchymal transition in sorafenib resistance hepatocellular carcinoma cells. [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 5639. doi:10.1158/1538-7445.AM2013-5639
Renal failure associated with low-molecular-weight dextran infusion.
Authors: T. O. Morgan, J. M. Little, W. A. Evans
Journal: BMJ (1966)

Treatment of Heart-block-El-Nahas and fohnson isuw 737 monitoring of the E.C.G., at least initially, an hourly pulse chart, and frequent E.C.G.s, while the dose is adjusted.The drug should be abandoned if it has insufficient effect to relieve Stoke-Adams attacks or failure, if it gives rise to unpleasant side-effects, or if the rate or rhythm is so unstable as to be intolerably disturbing or dangerous.