tbuckley/cabot-search huggingface dataset:
The Lewis A. Conner Memorial Lecture
Authors: JESSE E. EDWARDS
Journal: Circulation (1957)

While there are many anatomic varieties of congenital malformations of the heart and great vessels, most may be divided, from a functional point of view, into 3 types: (1) communication between the ventricles or between the aorta and pulmonary arteries, (2) anomalous drainage of pulmonary venous blood into the right atrium, and (3) obstruction to pulmonary venous flow. In each of these categories the responses of the pulmonary vascular tree have to be considered in understanding the altered dynamics. Depending on the type and degree of response in the pulmonary vascular bed, there may be a varying functional picture among patients having the same anatomic or functionally comparable malformation.
Differential response of human acute myeloid leukemia cells to gemtuzumab ozogamicin in vitro: role of Chk1 and Chk2 phosphorylation and caspase 3
Authors: Donatella Amico, Anna Maria Barbui, Eugenio Erba, Alessandro Rambaldi, Martino Introna, Josée Golay
Journal: Blood (2003)
The effect of lymphocytes from sufferers from recurrent aphthous ulceration upon colon cells in tissue culture
Authors: A. E. Dolby
Journal: Gut (1972)

The release of <sup>51</sup>Cr from labelled colon cells was used to assess a possible lymphocytotoxic effect of peripheral blood lymphocytes from patients suffering from recurrent aphthous ulceration. No significant (p &gt; 0·03) difference was observed between the isotope release following incubation with patients9 or control lymphocytes. The absence of such a lymphocytotoxic effect, detectable with oral epithelial cells, is discussed in relation to the role of cellular hypersensitivity in the pathogenesis of ulcerative colitis and aphthous ulceration.
On Antiseptic Inhalations
Authors: S. C. Smith
Journal: BMJ (1884)

JQOJqN4ywptqm, -of, dyspepsia; andd,often I payeJ,fund audible signs of diseAse where the patieilt has not comqp1aied of any cough whateve;In;;0her cses, ;when I have ,not been, able to satisfy my, earsj but fit sure, from the symptoms complained of, that mischief was brew- ing, the signs have at'last often become evident.Whenever we meet vith some of 'the early symptoms of phthisis in patients who have; hereditary.tendency to the disease, I think by far the safest plan is to treat4 the patient as if tse-lung-disease coild be distinctly heard.Now in this, the hereditary disease, I do not think that we have any specific remedy on which we can depend; but, at the same time,.we have a mode, of treating-these ;cases which often, when I have hardly hoped for,success, has proved very successful.andsatisfatory.In treating this disease, I am afraid we are all apt 'to' follow fashion -to piescribe romedies and modes of treatment at the time in vogue, and to forget the treatment which-sound common sense, combined with awreasonable' amount of medical knowledge, would dictate to us.The patienit should live in a part where the air .ispure, nieither too dry nor too moist, and where the climate pe,rmits out-door exercise to be.t4ken., Hence, removal to sqme of the places celebrated for this' clinmate,.is often of marked benefit, simply because the patient can then take plenty of exercise.
Total body skin examination for skin cancer screening in patients with focused symptoms
Authors: Giuseppe Argenziano, Iris Zalaudek, Rainer Hofmann-Wellenhof, Renato Marchiori Bakos, Wilma Bergman, Andreas Blum, Paolo Broganelli, Horacio Cabo, Filomena Caltagirone, Caterina Catricalà, Maurizio Coppini, Lucas Dewes, Maria Grazia Francia, Alessandro Garrone, Bengu Gerceker Turk, Giovanni Ghigliotti, Jason Giacomel, Jean-Yves Gourhant, Gerald Hlavin, Nicole Kukutsch, Dario Lipari, Gennaro Melchionda, Fezal Ozdemir, Giovanni Pellacani, Riccardo Pellicano, Susana Puig, Massimiliano Scalvenzi, Ana Maria Sortino-Rachou, Anna Rosa Virgili, Harald Kittler
Journal: Journal of the American Academy of Dermatology (2011)
Growth Failure, Deprivation, And Undereating
Authors: Charles F. Whitten
Journal: JAMA (1970)

To  Editor.—  Thompson and Blizzard have offered two criticisms of our paper relating to (1) the choice of  title, and (2) the conclusions reached. In our opinion, neither is valid.  The key word in  title is evidence , which our data do provide. The implication of  criticism is that we used  term proof. We did not.  In our communication only four statements of a concluding nature were made:   In this study, 11 of 13 infants gained weight at an accelerated rate during simultaneous understimulation and adequate feeding in  hospital. This is strong evidence that their poor weight status on admission was not emotionally induced but was  result of undereating.  Our evidence that underfeeding is  etiologic factor in  growth failure of maternally deprived infants is based entirely upon weight gain.  There are several mental-health implications of our finding that
Abstract 5316: GSK3β-dependent phosphorylation of LCRMP-1 is required for filopoda formation and tumor invasion
Authors: Wen-Lung Wang, Szu-Hua Pan, Yih-Leong Chang, Chen-Tu Wu, Yuh-Ling Chen, Tse-Ming Hong, Pan-Chyr Yang
Journal: Cancer Research (2012)

Abstract LCRMP-1, a novel isoform of CRMP-1, can promote cancer cell migration, invasion and associates with poor clinical outcome in patients with non-small cell lung cancer (NSCLC). However, the underlying mechanisms for regulation of LCRMP-1 in cancer cell invasiveness remain still obscure. Here, we report that GSK-3β can phosphorylate LCRMP-1 at Thr-628 in consensus sequences and this phosphrylation is crucial for function of LCRMP-1 on filopodia formation and cancer cell invasion. Impediment of Thr-628 phosphorylation attenuates the effects of LCRMP-1 to form filopodia and promote cancer invasion; simultaneously, kinase-dead GSK-3β diminishes regulation of LCRMP-1 on cancer cell invasion. Furthermore, we also found that patients with low-level inactive GSK-3β expression and high-level LCRMP-1 expression have worse overall survival than those with high-level inactive GSK-3β expressions and low-level LCRMP-1 expressions (P&amp;lt; 0.0001). Collectively, these results demonstrate that GSK-3β-dependent phosphorylation of LCRMP-1 provides an important mechanism for regulation of LCRMP-1 on cancer cell invasiveness and clinical outcome. 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 5316. doi:1538-7445.AM2012-5316
Corticosteroid-Induced Lymphopenia, Immunosuppression, and Body Defense
Authors: CHARLES G. CRADDOCK
Journal: Annals of Internal Medicine (1978)

The apparent paradox of heightened adrenal corticosteroid levels associated with reduction in the competence of the body's defensive apparatus to cope with exposure to new microbial antigens is considered. The question is asked how this lowered defensive capability, which occurs in the face of a threat to body integrity, is consistent with Cannon's principals of the "wisdom of the body." The suggestion is offered that the immunologic response to self-antigens exposed by disease or trauma may be suppressed by corticosteroid to offset the likelihood of autoimmune attack.
Abstract 3534: Epigenetic control of the tumor suppressive microRNA miR-34a in bladder cancer
Authors: Wen-Yu Huang, Pi-Che Chen, Chia-Ming Yeh, Frank H.C. Cheng, Hsiao-Yen Hsieh, Cheng-Huang Shen, Cheng-Da Hsu, Michael W. Chan
Journal: Cancer Research (2014)

Abstract Bladder cancer is the sixth most common cancer in the world and the incidence is particularly high in southwestern Taiwan. One of the hypotheses suggests that cancers arise from cancer stem-like cell (CSC) with surface antigen CD44. MicroRNAs (miRNAs) are endogenous, non-protein-coding RNAs that can regulate the expression of their target mRNAs. Up to 90% of human genes can be regulated by this mechanism. However, the role of miRNAs in the regulation of CSC in bladder cancer is not fully explored. Bioinformatics prediction identified that miR-34a regulates the expression of CD44. In this study, we aimed to investigate how miR-34a are regulated in bladder cancer. Expression analysis showed that miR-34a was down-regulated in UMUC3 bladder cancer cells. COBRA assay and bisulphite pyrosequencing demonstrated extensive DNA methylation of miR-34a in this cell. Treatment of DNMT inhibitor, 5-aza restored miR-34a expression in UMUC3 cells thus suggesting that miR-34a is epigenetically silenced in UMUC3 cells. Over-expression of miR-34a resulted in a reduction of chemo-resistance to cisplatin in UMUC3 cells. This may be due to a down-regulation of CD44 and another predicted miR-34a target, c-myc in this cell. Recently, additional mechanism namely, competitive endogenous RNA (ceRNA) hypothesis in controlling the function of miRNAs are demonstrated. To test this hypothesis in bladder cancer, we overexpressed 3′UTR of CD44 in TSGH8301 bladder cancer cells which expressed miR-34a, and resulted in an up regulation of another target of miR-34a, c-myc in this cells. Since amplification of chromosome 8q24 where c-myc resides is frequently observed in bladder cancer, we investigated the relationship between expression of c-myc and CD44 in a publicly available expression array data set (GDS1479) using 60 bladder cancer patients. Interestingly, a positive correlation was found between the expression of c-myc and CD44 (P=0.0016) in this data set. In conclusion, aberrant promoter methylation and ceRNA mechanism may contribute to attenuate the function of miR-34a in bladder cancer. The tumor suppressive role of miR-34a in controlling CSC phenotype in bladder cancer deserves further investigation. Citation Format: Wen-Yu Huang, Pi-Che Chen, Chia-Ming Yeh, Frank H.C. Cheng, Hsiao-Yen Hsieh, Cheng-Huang Shen, Cheng-Da Hsu, Michael WY Chan. Epigenetic control of the tumor suppressive microRNA miR-34a in bladder cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3534. doi:10.1158/1538-7445.AM2014-3534
Effects of chronic alcohol ingestion on myocardial lipid and fatty acid composition in adult turkeys
Authors: I. Soos, A. Facsko, I. Edes, E. Kiss, M. Csanady
Journal: Cardiovascular Research (1991)

The aim was determine whether alcohol induced left ventricular dilatation and myocardial lesions in turkeys are associated with changes in the phospholipid and fatty acid compositions of the cardiac tissue.Triglyceride, phospholipid, and cholesterol concentrations and the fatty acid compositions of phospholipids and triglycerides were measured in the myocardium of control and alcohol fed turkeys. Tissue samples were taken from the anteroapical wall of the left ventricle.Seven week old domestic Nicholas turkeys were used (10 controls and 10 ethanol fed); the alcohol, comprising more than 20% of the dietary energy, was given in the drinking water for 16 weeks.Left ventricular function was assessed by echocardiography at the end of the treatment. Different phospholipid fractions were isolated by two dimensional thin layer chromatography, and individual fatty acids were identified by gas chromatography. Non-invasive evaluation of the cardiac function revealed a dilatation of the left ventricle and an impaired contractile function in the alcoholic birds. Increased amounts of triglyceride, phosphatidylinositol, sphingomyelin, lysophosphatidylcholine, and lysophosphatidylethanolamine were found in the left ventricle of the alcoholic turkeys. Examination of the fatty acid compositions of different phospholipids and the triglyceride fraction revealed an increase in the saturated/unsaturated ratio following ethanol treatment. In the phospholipid fractions of the alcoholic birds the arachidonic acid (20:4n-6) content was significantly decreased as were the linolic (18:1) and linoleic (18:2n-6) acid contents in the triglycerides.These alterations in the myocardial phospholipid and fatty acid compositions may contribute to the electrophysiological and functional derangements of the left ventricle in alcoholic cardiomyopathy.
Obesity-induced inflammatory changes in adipose tissue
Authors: Kathryn E. Wellen, Gökhan S. Hotamisligil
Journal: Journal of Clinical Investigation (2003)

Obesity is associated with a state of chronic, low-grade inflammation. Two manuscripts in this issue of the JCI (see the related articles beginning on pages 1796 and 1821) now report that obese adipose tissue is characterized by macrophage infiltration and that these macrophages are an important source of inflammation in this tissue. These studies prompt consideration of new models to include a major role for macrophages in the molecular changes that occur in adipose tissue in obesity.
Warfarin Effect Enhanced by Disulfiram
Authors: Emil Rothstein
Journal: JAMA (1968)

To the Editor:—  Two drugs given together may antagonize or potentiate one another, have additive effects, increase combined therapeutic efficacy, or produce toxic conditions not associated with either alone. The chance of such occurrence is of course greater if their modes of action are related.  Disulfiram (Antabuse) and warfarin (Coumadin) sodium both act upon, or within, the liver cell. Disulfiram competes with nicotinamide adenine dinucleotide for the active centers of the enzyme aldehyde dehydrogenase, and also decreases the oxygen consumption and the xanthine oxidase, succinoxidase, and catalase activity of liver homogenates. 1 Warfarin inhibits enzyme systems in the liver cell which synthesize prothrombin. 1 No reports were found, in a rapid survey of the literature, of patients who received both drugs at the same time.  Report of a Case: —  A 45-year-old man with chronic alcoholism for 20 years, apparently secondary to a psychoneurotic anxiety reaction, was treated unsuccessfully for
Methodologic research needs in environmental epidemiology: data analysis.
Authors: R L Prentice, D Thomas
Journal: Environmental Health Perspectives (1993)

A brief review is given of data analysis methods for the identification and quantification of associations between environmental exposures and health events of interest. Data analysis methods are outlined for each of the study designs mentioned, with an emphasis on topics in need of further research. Particularly noted are the need for improved methods for accommodating exposure assessment measurement errors in analytic epidemiologic studies and for improved methods for the conduct and analysis of aggregate data (ecologic) studies.
Abstract 5462: MEDI3185, a potent anti-CXCR4 antibody, inhibits tumor cell migration, signaling and tumor growth in preclinical models.
Authors: Adeela Kamal, Youzhen Wang, Philipp Steiner, Anne-Marie Mazzola, Leslie Wetzel, Melissa Passino, Brenda McDermott, Keven Huang, Vahe Bedian, Norman Greenberg
Journal: Cancer Research (2013)

Abstract The chemokine receptor CXCR4 is a seven-transmembrane G-protein coupled receptor that mediates chemotaxis and cell migration upon stimulation via its ligand, stromal-derived factor 1 (SDF-1), also called CXCL12. CXCR4 is normally expressed on bone marrow stem and progenitor cells, various circulating lymphocytes, endothelial precursor cells, tissue macrophages and fibroblasts but the aberrant overexpression of CXCR4 is linked to various hematological malignancies, solid tumors and metastatic neoplasms. Moreover, CXCR4 overexpression is correlated with poor prognosis in many types of cancer, including breast, ovarian, colon, pancreatic, AML and glioblastomas. CXCR4 inhibition using siRNA, small-molecule and peptide inhibitors has demonstrated that it can inhibit tumor growth by blocking tumor cell survival/proliferation, metastasis, angiogenesis and tumor immune infiltrates. Here we describe a novel, fully human, antagonistic antibody to CXCR4, MEDI3185, which blocks SDF-1 binding to CXCR4. MEDI3185 has picomolar binding affinity to human CXCR4 and exhibits no significant binding to other chemokine receptors such as CCR4 or CXCR3. In vitro studies demonstrated that MEDI3185 inhibited tumor cell migration, blocked SDF-1 induced tumor cell signaling and induced apoptosis of tumor cells. In preclinical human tumor xenograft models in mouse, MEDI3185 showed single-agent tumor growth inhibition in multiple myeloma and B-cell Burkitt's lymphoma models and had combination activity in ovarian models. In addition, MEDI3185 extended survival as combination therapy in mouse models of CLL and also blocked lung tumor burden in a disseminated ovarian model. Combined, these data suggest that MEDI3185 is a potent CXCR4 antibody for the treatment of both hematological and solid tumors because it has pleiotropic effects on tumor biology that may enhance the efficacy of the current standard of care. Citation Format: Adeela Kamal, Youzhen Wang, Philipp Steiner, Anne-Marie Mazzola, Leslie Wetzel, Melissa Passino, Brenda McDermott, Keven Huang, Vahe Bedian, Norman Greenberg. MEDI3185, a potent anti-CXCR4 antibody, inhibits tumor cell migration, signaling and tumor growth in preclinical models. [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 5462. doi:10.1158/1538-7445.AM2013-5462
Efficacy of Ruxolitinib in Chronic Eosinophilic Leukemia Associated With a <i>PCM1-JAK2</i> Fusion Gene
Authors: Elisa Rumi, Jelena D. Milosevic, Ilaria Casetti, Irene Dambruoso, Daniela Pietra, Emanuela Boveri, Marina Boni, Paolo Bernasconi, Francesco Passamonti, Robert Kralovics, Mario Cazzola
Journal: Journal of Clinical Oncology (2013)
Abstract 10: Characterization of ovarian CSC using ALDH and CD133 identifies a cancer stem cell hierarchy
Authors: Ines A. Silva, Kun Yang, Karen Mclean, Tamara Minosyan, Greg Spalinger, Christophe Ginestier, Kevin Reynolds, Angie Kueck, Carolyn Johnston, Rebecca Liu, Max S. Wicha, Ronald J. Buckanovich
Journal: Cancer Research (2010)

Abstract Recent studies in ovarian cancer suggest that the protein CD133 may be a marker of cancer stem cells (CSC). CSC studies in several solid tumors have identified Aldehyde dehyrogenase (ALDH) enzymatic activity as a CSC marker, however ALDH has not been studied in ovarian cancer. We sought to determine if ALDH alone or in combination with CD133 could better define CSC in ovarian cancer. We analyzed the expression of these markers in 13 consecutive primary human ovarian tumor specimens and 8 cell lines. 70% of primary ovarian tumors analyzed had CD133+ cells detectable in low number in, and many tumor cell lines lacked CD133 expression. In contrast, 100% of the primary human ovarian tumor specimens and ovarian cancer cell lines demonstrated ALDH activity. ALDH+ cells isolated from 6 ovarian cancer cell lines preferentially grew larger tumors at a faster rate compared to ALDH− cells. In some cases ALDH− cells were incapable of generating tumors, suggesting ALDH is a good marker of ovarian CSC in cell lines. Importantly, as few as 1000 ALDH+ cells directly isolated from human ovarian tumors were capable of generating tumors in immune deficient mice. ALDH− cells did not form tumors in mice. Interestingly, when ALDH was used in combination with CD133 to analyze ovarian cancer cell lines we observed greater growth in the ALDH+CD133+ cells compared to ALDH+CD133− cells suggesting a potential hierarchy of the stem cells. Consistent with this, as few as 11 ALDH+CD133+ cells freshly isolated from human tumors were capable of forming tumors in mice. Consistent with a stem cell hierarchy, tumors formed from ALDH+CD133+ cells demonstrated a poorly differentiated histology, whereas tumors formed from ALDH+ cells alone demonstrated a more differentiated histology. Finally analysis of tumors generated from ALDH+ and ALDH+CD133+ tumors demonstrated a significant increase in microvascular density compared to ALDH− tumors. qRT-PCR analysis demonstrated that ALDH+ cells compared to ALDH− cells preferentially express numerous angiogenic factors. Taken together our studies: (1) indicate ALDH as a marker of ovarian CSC, (2) suggest a hierarchy of ovarian cancer stem cell differentiation state, and (3) demonstrates that ovarian CSC are highly angiogenic to recruit vasculature to create a stem cell niche. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 10.
HLA and ICAM-1 expression in alopecia areata<i>in vivo</i>and<i>in vitro</i>: the role of cytokines
Authors: A.J.G. MCDONAGH, J.A. SNOWDEN, C. STIERLE, K. ELLIOTT, A.G. MESSENGER
Journal: British Journal of Dermatology (1993)

To investigate the hypothesis that aberrant HLA and adhesion molecule expression in alopecia areata (AA) are secondary to local release of interferon-gamma (IFN-gamma) or other cytokines, we have studied HLA ABC, -DQ, -DR and ICAM-1 expression by immunohistochemistry, and compared patterns of expression in lesional tissue sections with those observed in hair follicles maintained in short-term organ culture, both from normal individuals and non-lesional sites in AA patients. The organ cultures were supplemented with IFN-gamma, tumour necrosis factor-alpha (TNF-alpha), and granulocyte-macrophage colony stimulating factor (GM-CSF), in a range of doses. In lesional AA tissue sections, there was close spatial correlation of ICAM-1 with HLA-DR; prominent staining being noted in the pre-cortical matrix and dermal papilla (DP) of lesional anagen follicles. In cultured follicles, dose-dependent induction of HLA class I, DR and ICAM-1 by IFN-gamma, and HLA class I and ICAM-1, but not HLA-DR, by TNF-alpha was observed in follicular epithelium, mainly in the outer root sheath (ORS). The findings in these cultures were the same in follicles derived from normal individuals and AA patients. Cytokine-induced patterns of HLA and ICAM-1 expression observed in vitro in cultured follicles differed significantly from those observed in vivo in lesional tissue sections. In particular, IFN-gamma failed to induce HLA-DR expression in the pre-cortical matrix and dermal papilla (DP), sites where this is usually observed in AA. The results suggest local cytokine release is not the sole determinant of aberrant HLA-DR expression in AA.
Use of Professional Time by Internists and General Practitioners in Group and Solo Practice
Authors: Barbara L. Brody, Joseph Stokes
Journal: Annals of Internal Medicine (1970)

The professional activities of 20 randomly-selected internists and general practitioners, in both group and solo practice in San Diego, Calif., were observed for 1 week in order to determine how they allocated their professional time. Time allocation varied markedly from one physician to another and was related both to specialty and type of practice. Most professional time was spent in direct patient contact (61.6%) and in other activities related to patient care (20.2%). The average physician spent only 14 min (3.1%) during the working day on all activities related to continuing education. General practitioners not only saw more patients but also spent less time in referring these patients to other physicians and in continuing education than did those practicing internal medicine. The data also suggest that those physicians who spend the most time in direct contact with patients also devote more time to the supervision of other health professionals.