tbuckley/cabot-search huggingface dataset:
COMPARATIVE CLINICAL EXPERIENCE WITH FIVE ANTIDEPRESSANTS
Authors: JOHN P. HOLT, ELEANORE R. WRIGHT, ARTHUR O. HECKER
Journal: American Journal of Psychiatry (1960)

Based on our results, we feel that all 5 of the antidepressants are effective agents and are generally superior to the amphetamines and phenothiazines in producing remission or relief of primary and secondary symptoms which comprise the depressive syndrome. Generally, the best response to the antidepressants occurs in patients with primary depressive reactions. Most patients with depressive features associated with schizophrenia or organic brain disorders experience significant improvement in depressive symptomatology without experience No serious complications or side effects were produced by the drugs. Postural hypotension, excessive psychomotor stimulation and aggravation of schizophrenic symptomatology were the most bothersome side effects and it would appear that each drug has a similar capacity to cause these reactions. Neither hemopoietic nor hepatic toxicity was evidenced during our experience with the drugs.
STAT5 regulation of BCL10 parallels constitutive NFκB activation in lymphoid tumor cells
Authors: Zsuzsanna S Nagy, Matthew J LeBaron, Jeremy A Ross, Abhisek Mitra, Hallgeir Rui, Robert A Kirken
Journal: Molecular Cancer (2009)

Signal Transducer and Activator of Transcription 5 A and B (STAT5) are key survival factors in cells of the lymphoid lineage. Identification of novel, tissue-specific STAT5 regulated genes would advance the ability to combat diseases due to aberrant STAT5 signaling. In the present work a library of human STAT5 bound genomic elements was created and validated. Of several STAT5 responsive genomic regulatory elements identified, one was located within the first intron of the human BCL10 gene. Chromatin immuno-precipitation reactions confirmed constitutive in vivo STAT5 binding to this intronic fragment in various human lymphoid tumor cell lines. Interestingly, non-phosphorylated STAT5 was found in the nuclei of Kit225 and YT cells in the absence of cytokine stimulation that paralleled constitutive NFκB activation. Inhibition of the hyperactive JAK3/STAT5 pathway in MT-2 cells via the Mannich-base, NC1153, diminished the constitutive in vivo occupancy of BCL10-SBR by STAT5, reduced NFκB activity and BCL10 protein expression in a dose dependent manner. Moreover, depletion of STAT5 via selective antisense oligonucleotide treatment similarly resulted in decreased BCL10 mRNA and protein expression, cellular viability and impaired NFκB activity independent of IL-2. These results suggest that the NFκB regulator BCL10 is an IL-2-independent STAT5 target gene. These findings proffer a model in which un-activated STAT5 can regulate pathways critical for lymphoid cell survival and inhibitors that disrupt STAT5 function independent of tyrosine phosphorylation may be therapeutically effective in treating certain leukemias/lymphomas.
Babington's aphasia--overcoming left hemisphere trauma
Authors: E H Jellinek
Journal: Journal of the Royal Society of Medicine (2003)

24 and a company commander in the 1st Dorset Regiment when he was wounded by shrapnel in Holland early in the morning of 2 November 1944, in the aftermath of the Arnhem campaign.His story is in his own writings 1,2 and in his army medical records 3 , both quite exceptional in detail and perception. CASE HISTORYHe was felled by the shell burst and briefly unconscious, and had sustained a left parietal penetrating injury which made him mute and hemiplegic.He was evacuated by stretcher, ambulance and plane.'During the flight I felt something stiff and cold on the right side of my chest.I puzzled about it for a while before it dawned on me that it was my right arm, heavy, insensate and quite paralysed . . .At one point I thought the end had come . ..' 2 .On the evening of the same day he reached the Military Hospital for Head Injuries at St Hugh's College, Oxford.X-rays showed 'a large MFB [metal foreign body] deep in the left parietal lobe just above the ventricular roof but may impinge on it.'On 3 November Major C A Calvert 4 operated on a semiconscious, globally aphasic man who had a right hemiplegia, hemianaesthesia, and hemianopia (Figure 1): '. . .wound stank horribly . . .contamination with hairs and dura down brain track-marked oedema . . .toothpaste brain and clot . . .bone chips indrawn about 2 cm, metallic body about 4 cm from cortex, inner end about 6 cm . . .debrided . . .many toothpaste pockets extending laterally from track . . .area of cortex destruction about 4 cmÂ4 cm . . .gush of CSF . . .ventricle into which MFB had protruded . . .5000 U penicillin . . .dura left open . . .drain . ..' 3 .After the operation Anthony Babington recalled 1,2 gesticulating with his left hand to indicate that he needed treatment for head pain, something to drink, or a urine bottle.When asked to write his home address with his left hand 'I knew exactly what I intended to write but I was dismayed to find myself drawing a series of short and very crooked lines . . .when shown a newspaper I could see letters but not understand them . . .might have been Chinese.'I woke one morning feeling slightly better.The night sister said ''You are over the worst and out of danger . . .The doctors think you might get back a little movement in your right side, in the leg at any rate.But I am afraid they think it unlikely that you will ever be able to speak again''.'
Identification of human urinary trefoil factor 1 as a novel calcium oxalate crystal growth inhibitor
Authors: S. Chutipongtanate
Journal: Journal of Clinical Investigation (2005)

Previous research on proteins that inhibit kidney stone formation has identified a relatively small number of well-characterized inhibitors. Identification of additional stone inhibitors would increase understanding of the pathogenesis and pathophysiology of nephrolithiasis. We have combined conventional biochemical methods with recent advances in mass spectrometry (MS) to identify a novel calcium oxalate (CaOx) crystal growth inhibitor in normal human urine. Anionic proteins were isolated by DEAE adsorption and separated by HiLoad 16/60 Superdex 75 gel filtration. A fraction with potent inhibitory activity against CaOx crystal growth was isolated and purified by anion exchange chromatography. The protein in 2 subfractions that retained inhibitory activity was identified by matrix-assisted laser desorption/ionization–time-of-flight MS and electrospray ionization–quadrupole–time-of-flight tandem MS as human trefoil factor 1 (TFF1). Western blot analysis confirmed the mass spectrometric protein identification. Functional studies of urinary TFF1 demonstrated that its inhibitory potency was similar to that of nephrocalcin. The inhibitory activity of urinary TFF1 was dose dependent and was inhibited by TFF1 antisera. Anti–C-terminal antibody was particularly effective, consistent with our proposed model in which the 4 C-terminal glutamic residues of TFF1 interact with calcium ions to prevent CaOx crystal growth. Concentrations and relative amounts of TFF1 in the urine of patients with idiopathic CaOx kidney stone were significantly less (2.5-fold for the concentrations and 5- to 22-fold for the relative amounts) than those found in controls. These data indicate that TFF1 is a novel potent CaOx crystal growth inhibitor with a potential pathophysiological role in nephrolithiasis.
Defective Mismatch Repair As a Predictive Marker for Lack of Efficacy of Fluorouracil-Based Adjuvant Therapy in Colon Cancer
Authors: Daniel J. Sargent, Silvia Marsoni, Genevieve Monges, Stephen N. Thibodeau, Roberto Labianca, Stanley R. Hamilton, Amy J. French, Brian Kabat, Nathan R. Foster, Valter Torri, Christine Ribic, Axel Grothey, Malcolm Moore, Alberto Zaniboni, Jean-Francois Seitz, Frank Sinicrope, Steven Gallinger
Journal: Journal of Clinical Oncology (2010)

Prior reports have indicated that patients with colon cancer who demonstrate high-level microsatellite instability (MSI-H) or defective DNA mismatch repair (dMMR) have improved survival and receive no benefit from fluorouracil (FU) -based adjuvant therapy compared with patients who have microsatellite-stable or proficient mismatch repair (pMMR) tumors. We examined MMR status as a predictor of adjuvant therapy benefit in patients with stages II and III colon cancer.MSI assay or immunohistochemistry for MMR proteins were performed on 457 patients who were previously randomly assigned to FU-based therapy (either FU + levamisole or FU + leucovorin; n = 229) versus no postsurgical treatment (n = 228). Data were subsequently pooled with data from a previous analysis. The primary end point was disease-free survival (DFS).Overall, 70 (15%) of 457 patients exhibited dMMR. Adjuvant therapy significantly improved DFS (hazard ratio [HR], 0.67; 95% CI, 0.48 to 0.93; P = .02) in patients with pMMR tumors. Patients with dMMR tumors receiving FU had no improvement in DFS (HR, 1.10; 95% CI, 0.42 to 2.91; P = .85) compared with those randomly assigned to surgery alone. In the pooled data set of 1,027 patients (n = 165 with dMMR), these findings were maintained; in patients with stage II disease and with dMMR tumors, treatment was associated with reduced overall survival (HR, 2.95; 95% CI, 1.02 to 8.54; P = .04).Patient stratification by MMR status may provide a more tailored approach to colon cancer adjuvant therapy. These data support MMR status assessment for patients being considered for FU therapy alone and consideration of MMR status in treatment decision making.
Hypothesis The Pruritus of Cholestasis: From Bile Acids to Opiate Agonists
Authors: Anthony E. Jones, Nora V. Bergasa
Journal: Hepatology (1990)

HepatologyVolume 11, Issue 5 p. 884-887 Special ArticleFree Access Hypothesis the pruritus of cholestasis: From bile acids to opiate agonists Dr. E. Anthony Jones, Corresponding Author Dr. E. Anthony Jones Liver Diseases Section, Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892Liver Diseases Section, Building 10, Room 4D52, National Institutes of Health, Bethesda, MD 20892===Search for more papers by this authorNora V. Bergasa, Nora V. Bergasa Liver Diseases Section, Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892Search for more papers by this author Dr. E. Anthony Jones, Corresponding Author Dr. E. Anthony Jones Liver Diseases Section, Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892Liver Diseases Section, Building 10, Room 4D52, National Institutes of Health, Bethesda, MD 20892===Search for more papers by this authorNora V. Bergasa, Nora V. Bergasa Liver Diseases Section, Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892Search for more papers by this author First published: May 1990 https://doi.org/10.1002/hep.1840110526Citations: 151AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume11, Issue5May 1990Pages 884-887 ReferencesRelatedInformation
A STUDY OF THE CIRCULATION OF THE KIDNEYS FOLLOWING LIGATION OF ONE URETER
Authors: Albert A. Ghoreyeb
Journal: The Journal of Experimental Medicine (1914)

During the first four or five days after ligation of the ureter, the changes in the kidney are mainly degenerative in type. One week after ligation of the ureter connective tissue cells begin to appear infiltrating the kidney tissues. There is also an increase in the vascular cells of the glomeruli. These changes are well marked at the end of twenty days from the time of ligation. At the end of twenty days from the time of ligation there is also a marked hypertrophy of the control kidney, the glomeruli showing an average increase in size of twenty-five microns.
P233 THE NATURAL COMPOUND PENTA-O-GALLOYL-GLUCOSE, DERIVED FROM THE ROOT CORTEX MOUTAN, EFFICIENTLY INHIBITS HEPATITIS C-VIRUS ENTRY AND SHOWS EXCELLENT PHARMACOKINETIC PERFORMANCE IN VIVO
Authors: P. Behrendt, E. Steinmann, A. Kusuma, P. Perin, N. Menzel, A. Ploss, P. Meulemann, M.P. Manns, T. Pietschmann
Journal: Journal of Hepatology (2014)
Attributions of Adolescents With Type 1 Diabetes in Social Situations
Authors: Anthony A. Hains, Kristoffer S. Berlin, W. Hobart Davies, Elaine A. Parton, Ramin Alemzadeh
Journal: Diabetes Care (2006)

To examine the relationships among negative attributions of friend reactions (NAFRs) within a social context, anticipated adherence difficulties, diabetes stress, and metabolic control.A sample of 104 adolescents with type 1 diabetes completed instruments measuring demographics, attribution of friend reactions, anticipated adherence, and diabetes stress. Metabolic control was measured by HbA(1c) obtained during the clinic visit.Path analysis demonstrated an excellent fit of a model depicting an indirect relationship between NAFRs and metabolic control through the mechanisms of expected adherence difficulties and diabetes stress.Adolescents who make NAFRs are likely to find adherence difficult in social situations and have increased feelings of stress, with the latter associated with poorer metabolic control. Intervention efforts to address negative attributions may impact adherence behavior and feelings of stress, especially if specific contexts of self-care behavior are taken into account.
An immunodominant class I-restricted cytotoxic T lymphocyte determinant of human immunodeficiency virus type 1 induces CD4 class II-restricted help for itself.
Authors: H Takahashi, R N Germain, B Moss, J A Berzofsky
Journal: The Journal of Experimental Medicine (1990)

We have observed that a peptide corresponding to an immunodominant epitope of the HIV-1 envelope protein recognized by class I MHC-restricted CD8+ CTL can also induce T cell help for itself. The help is necessary for restimulation of CTL precursors in vitro with peptide alone in the absence of exogenous lymphokines, can be removed by depletion of CD4+ T cells, and can be replaced by exogenous IL-2. Whereas the CTL in BALB/c or B10. D2 mice are restricted by the class I molecule Dd, the Th cells are restricted by the class II molecule Ad, and the help can be blocked by anti-Ad mAb. To examine the genetic regulation of the induction of help, we studied B10.A mice that share the class I Dd molecule, but have different class II molecules, Ak and Ek. Spleen cells of immune B10.A mice behave like CD4-depleted BALB/c spleen cells in that they cannot be restimulated in vitro by the peptide alone, but can with peptide plus IL-2. Therefore, in the absence of exogenous lymphokines, peptide-specific help is necessary for restimulation with this immunodominant CTL epitope peptide, and in H-2d mice, this peptide stimulates help for itself as well as CTL. We speculate on the implications of these findings for the immunodominance of this peptide in H-2d mice, and for the selective advantage of pairing certain class I and class II molecules in an MHC haplotype.
IL-17C is expressed in respiratory epithelial cells under inflammatory conditions
Authors: Philipp Pfeifer, Jan Hellberg, Philipp Lepper, Frank Langer, Robert Bals, Christoph Beisswenger
Journal: European Respiratory Journal (2012)

Background:  IL-17 is a cytokine that comprises a group of five IL-17 subtypes (IL-17 A to F). IL-17 directly activates epithelial cells leading to the expression of inflammatory mediators and antimicrobial factors. Recent studies showed that IL-17A/F is released by professional immune cells such as CD4+ T cells and macrophages whereas IL-17C is expressed by epithelial cells. It was the purpose of this study to examine the expression of IL-17 in respiratory epithelial cells infected with bacterial pathogens.   Methods:  Bronchial epithelial cells were exposed to smoke and infected with bacterial pathogens. Mice were exposed to smoke and colonized with  H. influenza . Expression and release of IL-17 (A to F) was measured by ELISA and qRT-PCR. IL-17C was detected in human bronchial tissue by immunohistochemistry.   Results:  Bacterial pathogens such as  P. aeruginosa  and  H. influenzae  induced the expression and release of IL-17C in human bronchial epithelial cells (HBECs). The same was true for ligands of Toll-like receptors 3 and 5 (flagellin, polyI:C). The expression of IL-17A/B/D/E was not induced by bacterial stimuli in HBECs. Cigarette smoke suppressed the expression of IL-17C in HBECs in response to bacterial infection in vitro and in the upper airways of mice colonized with  H. influenza  in vivo. IL-17C could be detected in bronchial tissue of subjects with infection-related lung diseases.   Conclusion:  These data show that IL-17C is involved in the innate immune response of respiratory epithelial cells. Smoke suppresses IL-17C expression in case of infection.
Plasma pro-surfactant protein B and lung function decline in smokers
Authors: Janice M. Leung, John Mayo, Wan Tan, C. Martin Tammemagi, Geoffrey Liu, Stuart Peacock, Frances A. Shepherd, John Goffin, Glenwood Goss, Garth Nicholas, Alain Tremblay, Michael Johnston, Simon Martel, Francis Laberge, Rick Bhatia, Heidi Roberts, Paul Burrowes, Daria Manos, Lori Stewart, Jean M. Seely, Michel Gingras, Sergio Pasian, Ming-Sound Tsao, Stephen Lam, Don D. Sin
Journal: European Respiratory Journal (2015)

Plasma pro-surfactant protein B (pro-SFTPB) levels have recently been shown to predict the development of lung cancer in current and ex-smokers, but the ability of pro-SFTPB to predict measures of chronic obstructive pulmonary disease (COPD) severity is unknown. We evaluated the performance characteristics of pro-SFTPB as a biomarker of lung function decline in a population of current and ex-smokers. Plasma pro-SFTPB levels were measured in 2503 current and ex-smokers enrolled in the Pan-Canadian Early Detection of Lung Cancer Study. Linear regression was performed to determine the relationship of pro-SFTPB levels to changes in forced expiratory volume in 1 s (FEV1) over a 2-year period as well as to baseline FEV1 and the burden of emphysema observed in computed tomography (CT) scans. Plasma pro-SFTPB levels were inversely related to both FEV1 % predicted (p=0.024) and FEV1/forced vital capacity (FVC) (p&lt;0.001), and were positively related to the burden of emphysema on CT scans (p&lt;0.001). Higher plasma pro-SFTPB levels were also associated with a more rapid decline in FEV1 at 1 year (p=0.024) and over 2 years of follow-up (p=0.004). Higher plasma pro-SFTPB levels are associated with increased severity of airflow limitation and accelerated decline in lung function. Pro-SFTPB is a promising biomarker for COPD severity and progression.
Induction of immunoglobulin gene expression in mouse fibroblasts by cycloheximide treatment.
Authors: T Ishihara, A Kudo, T Watanabe
Journal: The Journal of Experimental Medicine (1984)

A complete set of a rearranged human gamma 1-heavy chain gene, HIG1, was cloned from human plasma cell leukemia line, ARH-77, and transferred into mouse cells. It was strongly expressed in mouse myeloma cells but not in mouse L cells, indicating that immunoglobulin gene expression is not species-specific but cell-specific. However, a remarkable production of human gamma 1 chain was induced in mouse L cells containing HIG1 gene when the cells were treated with cycloheximide for a short period. The role of a labile repressor molecule in the expression of the immunoglobulin gene is proposed.
Neutrophil α-Defensins Cause Lung Injury by Disrupting the Capillary–Epithelial Barrier
Authors: Khalil Bdeir, Abd Al-Roof Higazi, Irina Kulikovskaya, Melpo Christofidou-Solomidou, Sergei A. Vinogradov, Timothy C. Allen, Steven Idell, Rose Linzmeier, Tomas Ganz, Douglas B. Cines
Journal: American Journal of Respiratory and Critical Care Medicine (2010)

The involvement of neutrophil activation in the sentinel, potentially reversible, events in the pathogenesis of acute lung injury (ALI) is only partially understood. alpha-Defensins are the most abundant proteins secreted by activated human neutrophils, but their contribution to ALI in mouse models is hindered by their absence from murine neutrophils and the inability to study their effects in isolation in other species.To study the role of alpha-defensins in the pathogenesis of ALI in a clinically relevant setting using mice transgenic for polymorphonuclear leukocyte expression of alpha-defensins.Transgenic mice expressing polymorphonuclear leukocyte alpha-defensins were generated. ALI was induced by acid aspiration. Pulmonary vascular permeability was studied in vivo using labeled dextran and fibrin deposition. The role of the low-density lipoprotein-related receptor (LRP) in permeability was examined.Acid aspiration induced neutrophil migration and release of alpha-defensins into lung parenchyma and airways. ALI was more severe in alpha-defensin-expressing mice than in wild-type mice, as determined by inspection, influx of neutrophils into the interstitial space and airways, histological evidence of epithelial injury, interstitial edema, extravascular fibrin deposition, impaired oxygenation, and reduced survival. Within 4 hours of insult, alpha-defensin-expressing mice showed greater disruption of capillary-epithelial barrier function and ALI that was attenuated by systemic or intratracheal administration of specific inhibitors of the LRP.alpha-Defensins mediate ALI through LRP-mediated loss of capillary-epithelial barrier function, suggesting a potential new approach to intervention.
EDHF and residual NO: different factors
Authors: B Vanheel
Journal: Cardiovascular Research (2000)

See article by Ge et al. [61] ( pages 547 -556) in thishyperpolarization in the rat aorta and pulmonary artery [4], issue.the rabbit femoral artery [5] or the dog mesenteric artery [6].Therefore, the existence of another relaxing factor, unrelated to NO and prostanoids, was proposed to contrib-1.Introduction ute to endothelium-mediated relaxations [4,7,8].This factor has been called endothelium derived hyperpolarizing The endothelium plays a pivotal role in the control of factor (EDHF).Later reports showed that inhibition of vascular tone and blood pressure.In response to a variety NOS had no effect on endothelium-dependent hyperpolariof physiological stimuli, such as bradykinin, acetylcholine, zation in the coronary artery [9,10], the rat mesenteric histamine, substance P, shear stress and pulsatile stretch, artery [11] and femoral vein [12].The importance of endothelial cells release vasodilator substances.Those EDHF in vasorelaxation was described to depend on the include prostacyclin [1] and endothelium-derived relaxing stimulus, the kind of vascular bed and the species under factor (EDRF) [2].The latter has been identified as nitric study.In several vascular beds, it has been shown that oxide (NO) [3].This labile compound is continuously endothelium-dependent EDHF-mediated relaxations insynthesized from L-arginine by the nitric oxide synthase crease with decreasing size of the vessel [13].Up to now, (NOS) enzyme constitutively expressed in the endothelial however, the chemical nature of this factor remains cell.It acts by direct stimulation of the soluble guanylyl elusive.Among possible candidates are epoxyeicosatcyclase in vascular smooth muscle cells.Since the elucida-rienoic acids (EETs) [14], which are cytochrome P450tion of the biosynthesis of NO, L-arginine analogues such derived metabolites of arachidonic acid, arachidonyl-etha-