tbuckley/cabot-search huggingface dataset:
Quality Assurance by Computerized Endoscopy Record Systems
Authors: F. M. Zwiebel, T. Sauerbruch
Journal: Endoscopy (1992)

Quality assurance in gastrointestinal endoscopy, as a crucial diagnostic and therapeutic process in medical care, has become a matter of increasing interest. However, concrete measures and standards are still lacking. Quality assurance as "continuous improvement" and "improvement by inspection" are discussed. Examples for clinical measures in the fields of indication for endoscopy, accuracy to the diagnostic test, thoroughness of the procedure and assessment of complications are given, and educational problems are discussed. Such structural problems of quality assurance as handling of a vast amount of data and assessment of late complications by follow-up information are addressed. Electronic data processing seems to be the most economic way to solve these problems. Requirements to data processing in the view of quality assurance are defined. Transferral of data from other departments within a hospital information system is necessary for the assessment of long-term follow-up. Different methods of communication within a hospital information system are discussed.
Effect of nifedipine on arterial hypoxaemia occurring after methacholine challenge in asthma.
Authors: E Ballester, J Roca, R Rodriguez-Roisin, A Agusti-Vidal
Journal: Thorax (1986)

To investigate whether the effects of nifedipine on methacholine induced broncho-constriction could impair pulmonary gas exchange in bronchial asthma a randomised, double blind, crossover study in 13 symptom free asthmatic subjects was designed. Each patient underwent a methacholine bronchial challenge test on two separate days one week apart, after having either oral nifedipine (20 mg thrice daily) or placebo for three days. Arterial blood gases were measured before and after methacholine challenge in nine subjects. Prechallenge values of forced expiratory volume in one second (FEV1) and arterial oxygen tension (Pao2) were similar after nifedipine and after placebo. After challenge, the cumulative doses of methacholine required to produce a 20% fall in FEV1 (PD20 FEV1) were significantly larger after nifedipine (280 (SD 347)) cumulative breath units (CBU) than after placebo (120 (183) CBU; p less than 0.01). After challenge the fall in Pao2 values (17.1 (1.6) mm Hg; (2.28 (0.21) kPa)) was significantly greater than after placebo (11.7 (2.4) mm Hg; (1.56 (0.32) kPa) p less than 0.03). Our data show that although oral nifedipine significantly reduces airway reactivity in patients with mild bronchial asthma, it also adversely affects pulmonary gas exchange, resulting in a lowered postchallenge Pao2, probably because of worsening ventilation-perfusion relationships.
S-Adenosylhomocysteine hydrolase activity in human myocardium
Authors: M. M Borst, A. Deussen, J. Schrader
Journal: Cardiovascular Research (1992)

Measurement of S-adenosylhomocysteine (SAH) accumulation in the heart reflects the concentration of free cytosolic adenosine and is thus a sensitive indicator of regional myocardial ischaemia. To evaluate the possibility of applying this method in combination with 11C-SAH positron emission tomography (PET) to patients with ischaemic heart disease the activity of SAH hydrolase in human heart muscle and its regional distribution were studied.Myocardium from patients with dilated cardiomyopathy (n = 4), hypertrophic obstructive cardiomyopathy (HOCM, n = 6), and mitral stenosis (n = 3) was analysed. Additional studies were performed in myocardium, isolated cardiomyocytes, and endothelial cells from dog and guinea pig hearts. Enzyme activity in synthetic and hydrolytic direction including kinetic data (Vmax, KM values, pH dependency) was measured in the cytosolic fraction of myocardial tissue and cell extracts, using high performance liquid chromatography and photometric methods, respectively.Rates of SAH synthesis (Vmax) in the left ventricle in dilated cardiomyopathy, mitral stenosis, and HOCM were 0.8 (SEM 0.1), 1.0(0.2), and 1.7(0.1) nmol.min-1.mg-1 protein respectively. KM values for DL-homocysteine, adenosine, and SAH in HOCM were 187, 2.2, and 3.4 microM, respectively. Enzyme activity was homogeneously distributed among right and left atria, right and left ventricles, and septum. Additional studies in homogenated muscle and isolated cardiomyocytes of guinea pig and canine hearts showed activities similar to man.(1) SAH hydrolase activity in the human heart is quantitatively comparable to that found in other mammals but certain myocardial diseases may go along with changes in SAH hydrolase activity; (2) the kinetic properties, absolute amounts, and homogeneous distribution of the enzyme may permit the non-invasive determination of free adenosine in the human heart by PET.
Delayed Visualization of the Gallbladder with a Rim Sign
Authors: PATRICIA A. LOWRY, HUYEN D. TRAN
Journal: Clinical Nuclear Medicine (1991)

The rim sign of increased activity in the gallbladder fossa during nuclear hepatobiliary imaging has been described, with one exception, only in conjunction with a nonvisualizing gallbladder, and it strongly suggests acute complicated cholecystitis. A case is presented in which a rim sign was present despite later visualization of the gallbladder in presumed chronic cholecystitis.
226 ACUTE AND 14-DAYS HEPATIC VENOUS PRESSURE GRADIENT RESPONSE TO CARVEDILOL AND NEBIVOLOL IN PATIENTS WITH LIVER CIRRHOSIS. A PILOT STUDY
Authors: V. Silkauskaite, A. Pranculis, J. Kupcinskas, V. Petrenkiene, L. Kupcinskas
Journal: Journal of Hepatology (2009)
Brief report: Pure red cell aplasia following pernicious anemia
Authors: Kazuo Dan, Toshiharu Ito, Takeo Nomura
Journal: American Journal of Hematology (1990)

Abstract A rare case of pure red cell aplasia (PRCA) in association with pernicious anemia is reported. A 40‐year‐old man presented with typical clinical and laboratory features of pernicious anemia and received intramuscular injections of vitamin B 12 , with satisfactory response. Anemia recurred 6 months later despite continued therapy, and the patient was noted to have PRCA, which was treated successfully with two courses of high‐dose bolus methylprednisolone therapy. His peripheral mononuclear cells before the therapy suppressed colony formation of early erythroid precursors (BFU‐E) from normal bone marrow; such a suppressive effect was not found after recovery from anemia.
Toward a 21st Century Health System: The Contributions and Promise of Prepaid Group Practice
Authors: David Woods
Journal: BMJ (2004)

Managed care, which stemmed the annual rise in healthcare costs in the United States from a high of around 18% to something closer to 4%, may be losing steam, as those increases are now back into double digits. An alternative, according to the more than 20 contributors to this book, is prepaid group practice (PGP). A PGP is “an integrated entity that includes both a healthcare delivery system (doctors, other clinicians, laboratories, clinics, and hospitals) and an insurance function (financing arrangements, benefit plans, marketing, and customer service systems) ‘under one roof.’” Its main components are professionals from various specialties, a voluntarily enrolled population, comprehensive service, prepayment by people enrolling, and accountability for the …
Abstract 1676: Chemotherapy-induced immunogenic modulation of tumor cells enhances killing by cytotoxic T lymphocytes and is distinct from immunogenic cell death.
Authors: James W. Hodge, Charlie T. Garnett, Benedetto Farsaci, Claudia Palena, Kwong-Yok Tsang, Soldano Ferrone, Sofia R. Gameiro
Journal: Cancer Research (2013)

Abstract Certain chemotherapeutic regimens trigger cancer cell death while inducing dendritic cell maturation and subsequent immune responses. However, chemotherapy-induced immunogenic cell death (ICD) has thus far been restricted to select agents. In contrast, several chemotherapeutic drugs modulate antitumor immune responses, despite not inducing classic ICD. In addition, in many cases tumor cells do not die after treatment. Here, using docetaxel, one of the most widely used cancer chemotherapeutic agents, as a model, we examined phenotypic and functional consequences of tumor cells that do not die from immunogenic cell death. Docetaxel treatment of tumor cells did not induce ATP or HMGB1 secretion, or cell death. However, calreticulin exposure was observed in all cell lines examined after chemotherapy treatment. Killing by CEA, MUC-1, or PSA-specific CD8+ CTLs was significantly enhanced after docetaxel treatment. This killing was associated with increases in components of antigen-processing machinery, and mediated largely by calreticulin membrane translocation, as determined by functional knockdown of calreticulin, PERK, or calreticulin-blocking peptide. A docetaxel-resistant cell line was selected (MDR-1+, CD133+) by continuous exposure to docetaxel. These cells, while resistant to direct cytostatic effects of docetaxel, were not resistant to the chemomodulatory effects that resulted in enhancement of CTL killing. Here, we provide an operational definition of “immunogenic modulation,” where exposure of tumor cells to nonlethal/sublethal doses of chemotherapy alters tumor phenotype to render the tumor more sensitive to CTL killing. These observations are distinct and complementary to immunogenic cell death and highlight a mechanism whereby chemotherapy can be used in combination with immunotherapy. Citation Format: James W. Hodge, Charlie T. Garnett, Benedetto Farsaci, Claudia Palena, Kwong-Yok Tsang, Soldano Ferrone, Sofia R. Gameiro. Chemotherapy-induced immunogenic modulation of tumor cells enhances killing by cytotoxic T lymphocytes and is distinct from immunogenic cell death. [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 1676. doi:10.1158/1538-7445.AM2013-1676
Gallium-67 Uptake in a Benign Thymic Cyst
Authors: STEVEN R. JENSEN, B RAMA RAO, JAMES W. WINEBRIGHT, RICHARD O??REILLY
Journal: Clinical Nuclear Medicine (1980)

JENSEN, STEVEN R. LT. M.C., U.S.N.R.; RAO, B RAMA CDR M.C., U.S.N.; WINEBRIGHT, JAMES W. CAPT. M.C., U.S.N.; O'REILLY, RICHARD CAPT. M.C., U.S.N. Author Information
TECHNETIUM-99m DTPA AND I-125 IOTHALAMATE PLASMA CLEARANCES IN DIABETIC PATIENTS
Authors: B. Y. Croft, F. Pauley, L. Noland, C. D. Teates, W. K. Bolton
Journal: Clinical Nuclear Medicine (1988)

The renal clearance of I-125 iothalamate is a recognized method for estimating GFR, using a constant infusion technique. In diabetic patients, the urinary bladder may not be emptied when urinary sampling is performed. If retained urine volume does not remain constant, the estimation of flow rate in the interval is incorrect. The purpose of this study was to compare Tc-99m DTPA and I-125 iothalamate clearances in diabetic patients, and to assess the effect of retained urine on GFR. Tc-99m DTPA and I-125 iothalamate were infused for simultaneous GFR measurements and estimation of retained urine in 4 intervals each in 12 patients. Retained urine was estimated by Anger camera imaging and computer storage of Tc-99m bladder images. Corrections were made for the time elapsed between voiding and imaging. Tc-99m DTPA urine cpm/ml: plasma cpm/ml ratios correlated well with I-125 iothalamate values: intercept=-.13, slope=.954, and r=.987. The average of 44 intervals of retained urine was 75±72 ml (range 0 - 225), while the average volume voided was 254±147 ml (range 0 - 640). Patients with > 50 ml retained had 20±27% variation in urine flow vs 6±4% for those with <50 ml; variation in GFR was 68±30% for retainers vs 25±12% for nonretainers. Steady state GFR in retainers was 73±14 vs 82±17 ml/min for non-retainers, by iothalamate. For GFR estimation, Tc-99m DTPA is equivalent to I-125 iothalamate and can be used to make retained urine corrections in diabetic patients.
A randomized trial of dasatinib 100 mg versus imatinib 400 mg in newly diagnosed chronic-phase chronic myeloid leukemia
Authors: Jerald P. Radich, Kenneth J. Kopecky, Frederick R. Appelbaum, Suzanne Kamel-Reid, Wendy Stock, Greg Malnassy, Elisabeth Paietta, Martha Wadleigh, Richard A. Larson, Peter Emanuel, Martin Tallman, Jeff Lipton, A. Robert Turner, Michael Deininger, Brian J. Druker
Journal: Blood (2012)
Effect of lung T lymphocytes on fibroblasts in idiopathic pulmonary fibrosis and extrinsic allergic alveolitis.
Authors: M Selman, G Gonzalez, M Bravo, J Sullivan-Lopez, C Ramos, M Montano, N Barquin, F Vadillo
Journal: Thorax (1990)

Increased fibroblast replication and interstitial collagen accumulation occur commonly in the interstitial lung disease that progress to fibrosis. The processes controlling lung fibrogenesis are not completely understood, however. This study was designed to analyse the influence of T lymphocytes from lung tissue obtained at open lung biopsy from four patients with idiopathic pulmonary fibrosis and four patients with extrinsic allergic alveolitis on fibroblast proliferation and collagen synthesis in vitro. Lung T cell supernatants from patients with both diseases induced a moderate but significant inhibition of human lung fibroblast cell line growth. In contrast, there was a clear difference in the effect of T cells from the two groups of patients in relation to collagen production. Lung T lymphocytes from all four patients with idiopathic pulmonary fibrosis produced a substantial increase in collagen synthesis (from 371% to 514% of control values), whereas T cells from three of the four patients with extrinsic allergic alveolitis induced a significant decrease in collagen production (to 35%, 36%, and 43% of control values); in the fourth case there was an increase in collagen synthesis but this was lower than that seen with T cells from any of the patients with idiopathic pulmonary fibrosis. Peripheral T cells from six patients and control subjects caused a small increase in fibroblast proliferation and no change in collagen synthesis. The findings suggest that at least two types of interaction occur between lung T cells and fibroblasts in these disorders. A variable degree of inhibition of cell proliferation is observed in response to lung T cell supernatants from patients with both idiopathic pulmonary fibrosis and extrinsic allergic alveolitis; a substantial increase in collagen synthesis is triggered by lymphokines from patients with idiopathic pulmonary fibrosis.
Vision from next generation sequencing: Multi-dimensional genome-wide analysis for producing gene regulatory networks underlying retinal development, aging and disease
Authors: Hyun-Jin Yang, Rinki Ratnapriya, Tiziana Cogliati, Jung-Woong Kim, Anand Swaroop
Journal: Progress in Retinal and Eye Research (2015)

Genomics and genetics have invaded all aspects of biology and medicine, opening uncharted territory for scientific exploration. The definition of "gene" itself has become ambiguous, and the central dogma is continuously being revised and expanded. Computational biology and computational medicine are no longer intellectual domains of the chosen few. Next generation sequencing (NGS) technology, together with novel methods of pattern recognition and network analyses, has revolutionized the way we think about fundamental biological mechanisms and cellular pathways. In this review, we discuss NGS-based genome-wide approaches that can provide deeper insights into retinal development, aging and disease pathogenesis. We first focus on gene regulatory networks (GRNs) that govern the differentiation of retinal photoreceptors and modulate adaptive response during aging. Then, we discuss NGS technology in the context of retinal disease and develop a vision for therapies based on network biology. We should emphasize that basic strategies for network construction and analyses can be transported to any tissue or cell type. We believe that specific and uniform guidelines are required for generation of genome, transcriptome and epigenome data to facilitate comparative analysis and integration of multi-dimensional data sets, and for constructing networks underlying complex biological processes. As cellular homeostasis and organismal survival are dependent on gene-gene and gene-environment interactions, we believe that network-based biology will provide the foundation for deciphering disease mechanisms and discovering novel drug targets for retinal neurodegenerative diseases.
Hepatic Photopenia in Gallium Imaging
Authors: ANNE M. GLASER, DAVID C. P. CHEN, MICHAEL E. SIEGEL
Journal: Clinical Nuclear Medicine (1988)

Although Ga-67 has been used extensively in Imaging many different conditions, much is yet unknown about the mechanisms by which gallium concentrates preferentially in tissues such as the liver. This paper reports three patients with markedly diminished hepatic uptake of gallium. The cases are examined in light of published data demonstrating such factors as transferrin levels, radiation, and chemotherapeutic agents as altering the hepatic uptake of gallium. Of the many factors believed to influence the biodistribution of gallium, none can definitively account for the lack of hepatic uptake in these patients.
Cellular and molecular mechanisms of endothelial cell dysfunction.
Authors: D G Harrison
Journal: Journal of Clinical Investigation (1997)

repeated observation that it is altered by a variety of pathophysiological conditions. Such alterations of NO production and/or bioavailability have been shown to occur both in experimental animal models and in human subjects, in the setting of such diverse disorders as hypertension, hypercholesterolemia, aging, cigarette smoking, diabetes, and heart failure (1). The mechanisms underlying the alteration of this important function of the endothelium are varied and likely multifactorial. During the past several years an enormous amount of research has been devoted to understanding these abnormalities, which has led to new insights into regulation of vascular tone, redox state, inflammation, growth, and the prothrombotic/antithrombotic properties of the vessel wall. This Perspective will highlight some of these important new observations, as they relate to the pathology of the endothelial cell L -arginine/NO synthase (NOS) system. In addition, future directions of research that may be particularly informative will be indicated. Alterations of the substrate for the NOS enzyme The substrate for NOS is the basic amino acid L -arginine (with a K m of approximately 5 m M, reference 2). L -Arginine is syn
Infection After Splenectomy
Authors: Richard Platt
Journal: JAMA (1982)

Postsplenectomy infection has engaged the attention of physicians at least since 1919.<sup>1</sup>Publications on the role of the spleen or the sequelae of its absence continue to appear almost weekly. After decades of interest, what do we know about the risk of infection after splenectomy? We seem to know that young children experience a high attack rate, particularly of fulminant infections caused by encapsulated organisms. We have suspected the same thing about adults, although the evidence for this conclusion has been much less secure. There has been general but not universal agreement that adults have a higher-than-normal risk of infection after splenectomy, and also that the magnitude of this risk varies with the reason for splenectomy. However, the measured or inferred risk estimates cover a very wide range.<sup>2-4</sup>Schwartz and colleagues have provided several useful observations in their article, which appears in this issue (p 2279). The risk
Effects of Heparin and ε-Aminocaproic Acid in Dogs on Plasmin- 125I Generation in Response to Urokinase Injections and Venous Injury
Authors: Y. Takeda, T. R. Parkhill, M. Nakabayashi
Journal: Journal of Clinical Investigation (1972)

The isotopic method described previously for quantification of plasmin- (125)I by disc gel electrophoresis was modified by inclusion of euglobulin precipitation to expand its applicability to plasmas containing low radioactivity of plasmin- (125)I and plasminogen- (125)I. It was found that the euglobulin precipitation method precipitates 72.4+/-2.1 (sd)% of both plasmin- (125)I and plasminogen- (125)I. Using this method and plasminogen- (125)I as a tracer, studies were first made of the effects of heparin and epsilon-aminocaproic acid in dogs on plasmin- (125)I generation in responese to a single injection of urokinase and to venous injury; second, of the effects of venous occlusion and thrombosis on plasmin- (125)I generation; and third, in vitro studies of plasminogen- (125)I affinity to fibrin and its activation in blood clots. The venous injury was produced by the damage of venous endothelium by an injection of 90% phenol and the thrombosis by a thrombin injection into an occluded vein. Heparin and epsilon-aminocaproic acid under the present experimental conditions inhibited about 78 and 100%, respectively of plasmin- (125)I generation by the urokinase injection. Similar inhibitory effects of heparin and epsilon-aminocaproic acid were observed on plasmin- (125)I generation in response to venous injury. The venous occlusion caused a small degree of plasmin- (125)I generation, but thrombin thrombosis did not seem to stimulate the generation of plasmin- (125)I. The in vitro studies showed that plasminogen- (125)I does not have a specific affinity to fibrin and is incorporated into blood clots in approximately equal concentrations as those in serum during clotting processes, and that blood clots per se do not stimulate plasmin- (125)I generation. These results suggest that injured veins release considerable amounts of vascular plasminogen activators into circulation and that these play an important role in thrombus dissolution in vivo.
Human Organ Support and Replacement: Transplantation and Artificial Prostheses
Authors: Alan Marty
Journal: JAMA (1972)

This clinically oriented survey of the recent advances in human organ transplantation and prostheses will appeal to all workers in these fields. Each contributor keeps to his editorial assignment and exposes the reader to all major developments in the field through 1969. By presenting in one volume knowledge about both artificial organ support and transplantation, Dr. Hardy appropriately integrates these previously divergent fields. Some of the outstanding achievements of this volume include Carpentier and Dubost's chapter on allograft and xenograft heart valves, Hardy's chapters on heart and lung transplantation, Manax and Lillehei's discussion of gastric and intestinal transplantation, Bigelow and Starr's chapter on prosthetic cardiac valves, and Wesolowski's discussion of blood vessel replacement. Separate chapters on the transplantation of each visceral organ serve as possible sources of wider benefit; for example, the kidney transplanter may benefit from reading John Norman's review of the problems encountered in splenic transplantation. Extracorporeal support
Erratum to “Intracellular distribution of NFκB decoy and its inhibitory effect on TNFα production by LPS stimulated RAW 264.7 cells” [J. Control. Release 107(2005) 373–382]
Authors: Yuriko Higuchi, Shigeru Kawakami, Makiya Nishikawa, Fumiyoshi Yamashita, Mitsuru Hashida
Journal: Journal of Controlled Release (2006)
GW25-e3197 β1-adrenoceptor Autoantibodies Affect Action Potential Duration and Delayed Rectifier Potassium Currents in Guinea Pigs
Authors: Zhao Yuhui, Haixia Huang, Yunhui Du, Xiao Li, Tingting Lv, Suli Zhang, Hua Wei, Jianyu Shang, Ping Liu, Huirong Liu
Journal: Journal of the American College of Cardiology (2014)
The Lewis A. Conner Memorial Lecture
Authors: DICKINSON W. RICHARDS
Journal: Circulation (1953)

Dyspnea has many characteristics, differing from one clinical state to another. In pulmonary diseases the immediate cause is usually a disproportion between actual ventilation (breathing requirement) and breathing capacity. The hyperventilation of organic pulmonary disease is often mistakenly diagnosed as psychoneurosis. In early cardiac dyspnea, muscular fatigue associated with inadequate cardiac output may be a factor. True pulmonary congestion becomes important in more advanced left ventricular failure.