tbuckley/cabot-search huggingface dataset:
Energy metabolism in patients with acute and chronic liver disease
Authors: Bruno Schneeweiss, Wolfgang Graninger, Peter Ferenci, Sabine Eichinger, Georg Grimm, Barbara Schneider, Anton N. Laggner, Kurt Lenz, Gunter Kleinberger
Journal: Hepatology (1990)

Energy expenditure and substrate oxidation rate for fat, glucose and protein were evaluated by indirect calorimetry in 20 normal individuals, 35 patients with acute hepatitis and 22 patients with biopsyproven alcoholic cirrhosis in the postabsorptive state. Measurements were done in the resting state after an overnight fast (10 to 12 hr). Oxygen consumption (ml/min/1.73 m2) in normal subjects, in patients with acute hepatitis and in patients with cirrhosis was 206.5 ± 4.0 (mean ± S. E. M.), 216.4 ± 4.7 and 228.8 ± 7.1 (p < 0.05 vs. controls), respectively. When related to body surface area (Kcal/min/1.73 m2), resting energy expenditure did not differ between normal subjects (0.98 ± 0.02), patients with acute hepatitis (1.03 ± 0.02) and cirrhotic patients (1.06 ± 0.03). However, when related to 24-hr urinary creatinine excretion as an estimate of lean body mass, energy expenditure was in creased in cirrhosis (p < 0.0001). In cirrhosis an inverse association between the severity of liver disease according to Pugh and oxygen consumption and resting energy expenditure was found. In cirrhotic patients the percentages of total calories derived from fat (86% ± 5%), carbohydrate (2% ± 4%) and protein (12% ± 1%) were different from those of normal controls who metabolized 45% ± 4%, 38% ± 4%, 17% ± 1%, respectively. In acute hepatitis no alterations in metabolism could be found apart from a decreased protein oxidation rate. In conclusion no appreciable changes in energy metabolism exist in acute hepatitis. The pattern of fuel use in cirrbosis resembles that in starvation. Data on resting energy expenditure depend on the calculations used. Resting energy expenditure was not increased in either group when related to body surface area. An inverse association between the severity of liver disease and energy expenditure was found in cirrhosis. (HEPATOLOGY 1990;11:387–393.)
Irregular regeneration of hepatocytes and risk of hepatocellular carcinoma in chronic hepatitis and cirrhosis with hepatitis-C-virus infection
Authors: Minoru Shibata, Toshio Morizane, Toshikazu Uchida, Tomoyuki Yamagami, Yasushi Onozuka, Masayuki Nakano, Keiji Mitamura, Yukihisa Ueno
Journal: The Lancet (1998)
Cardiac Hydatid Cysts
Authors: D. S. Gibson
Journal: Thorax (1964)

There is an increasing number of reports in the literature of cases of primary echinococcosis of the heart which have been treated surgically.Prior to 1932, when Long performed the first successful operation, these cysts were nearly always diag- nosed in the post-mortem room.Until 1947 only four successful cases had been reported.Since that time there have been another 42 cases in the world, of which all but seven have been reported as cured.The following are two cases successfully treated by operation.CASE REPORTS CASE 1 Mrs. B. M. S. aged 23 years was referred to the Thoracic Surgical Clinic of the Royal Hobart Hospital on 18 April 1961 for investigation of a lesion seen in a plain radiograph of the chest (Fig. 1) which had been taken when she had complained of pains in the breasts.This radiograph showed a calci- fied shadow at the apex of the left ventricle.She had no complaints other than those related to the breasts; her general health was good; she had a normal exercise tolerance and had no cough..1 FIG. 1. Case 1.-The calcified rim can be seen at the apex of the heart.
Inhibitory Effects of Transforming Growth Factor β1 on Mitogenic Response, Transforming Growth Factor α, and c-myc in Quiescent, Well-Differentiated Colon Carcinoma Cells
Authors: Kathleen M. Mulder, Qing Zhong, Ho Gene Choi, Lisa E. Humphrey, Michael G. Brattain
Journal: Cancer Research (1990)

Previously, we reported that exponentially proliferating cultures of well-differentiated human colon carcinoma cells responded to transforming growth factor β1 (TGF-β) with growth inhibition, alterations in morphology, and increased secretion of the differentiation marker, carcinoembryonic antigen. Poorly differentiated cultures were unresponsive. Here we show that TGF-β was ineffective in repressing nutrient-stimulated mitogenesis in quiescent, poorly differentiated cells. However, in quiescent, well-differentiated cells, TGF-β repressed the mitogenic responses to both nutrients alone (by 90%) and to nutrients plus the exogenous stimulatory factors epidermal growth factor (E), insulin (I), and transferrin (T) (by 55–65%). Thymidine incorporation experiments indicated that TGF-β reduced both the onset and peak mitogenic response to growth factors and/or nutrients in the well-differentiated cells. Additionally, TGF-β repressed the growth factor (E + I + T)-stimulated up-regulation of expression of both c- myc and of transforming growth factor α (TGF-α) mRNAs in quiescent, well-differentiated cells. TGF-β also elicited a rapid ( t ½ ≈1h) down-regulation of c- myc expression in the absence of prior growth factor (E + I + T) stimulation. In contrast, TGF-β had no effect on c- myc or TGF-α mRNA expression in the poorly differentiated cells. The results suggest that TGF-β exerts rapid inhibitory effects on proliferation-associated genes in quiescent and restimulated, well-differentiated cells. Expression of these genes (c- myc and TGF-α) may otherwise (in the absence of TGF-β) play roles in the cellular signaling of mitogenic responses by growth stimulatory factors in well-differentiated colon carcinoma cells.
Ischemic Stroke Therapy
Authors: C. Stapf, J. P. Mohr
Journal: Annual Review of Medicine (2002)

▪ Abstract Stroke is the most common life-threatening neurologic disease and the leading cause of serious long-term disability. The advent of new treatment options for selected patients suffering ischemic stroke (such as systemic administration of tissue plasminogen activator or catheter-guided intra-arterial thrombolysis), the structural reorganization of patient care facilities into stroke units, and interdisciplinary cerebrovascular centers have broadened the scope of possible therapeutic interventions in the acute and postacute phase after cerebral ischemia. This review summarizes currently available and recommended treatment modalities for acute ischemic stroke from an interdisciplinary perspective, including medical, neurointerventional, and neurosurgical therapies.
A puzzling mutation in congenital erythropoietic porphyria and an association with β-thalassaemia trait
Authors: J.E. Maakaron, O. Abdel Malak, S. Itani, M.D. Cappellini, E. Di Pierro, V. Brancaleoni, F. Granata, A.T. Taher
Journal: British Journal of Dermatology (2012)

Journal Article A puzzling mutation in congenital erythropoietic porphyria and an association with β‐thalassaemia trait Get access J.E. Maakaron, J.E. Maakaron Department of Internal Medicine, Division of Hematology and Oncology, American University of Beirut Medical Center, PO Box 11‐0236, Riad El‐Solh, 1107 2020 Beirut, Lebanon Search for other works by this author on: Oxford Academic Google Scholar O. Abdel Malak, O. Abdel Malak Faculty of Medicine, American University of Beirut, Beirut, Lebanon Search for other works by this author on: Oxford Academic Google Scholar S. Itani, S. Itani Department of Dermatology, American University of Beirut Medical Center, Beirut, Lebanon Search for other works by this author on: Oxford Academic Google Scholar M.D. Cappellini, M.D. Cappellini Dipartimento di Medicina Interna, Fondazione IRCCS ‘Ca Granda’, Ospedale Maggiore Policlinico, Università degli Studi di Milano, Milan, Italy Search for other works by this author on: Oxford Academic Google Scholar E. Di Pierro, E. Di Pierro Dipartimento di Medicina Interna, Fondazione IRCCS ‘Ca Granda’, Ospedale Maggiore Policlinico, Università degli Studi di Milano, Milan, Italy Search for other works by this author on: Oxford Academic Google Scholar V. Brancaleoni, V. Brancaleoni Dipartimento di Medicina Interna, Fondazione IRCCS ‘Ca Granda’, Ospedale Maggiore Policlinico, Università degli Studi di Milano, Milan, Italy Search for other works by this author on: Oxford Academic Google Scholar F. Granata, F. Granata Dipartimento di Medicina Interna, Fondazione IRCCS ‘Ca Granda’, Ospedale Maggiore Policlinico, Università degli Studi di Milano, Milan, Italy Search for other works by this author on: Oxford Academic Google Scholar A.T. Taher A.T. Taher Department of Internal Medicine, Division of Hematology and Oncology, American University of Beirut Medical Center, PO Box 11‐0236, Riad El‐Solh, 1107 2020 Beirut, Lebanon A.T. Taher. E‐mail: ataher@aub.edu.lb Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 167, Issue 3, 1 September 2012, Pages 697–699, https://doi.org/10.1111/j.1365-2133.2012.10954.x Published: 01 September 2012
New Strategies in Lung Cancer: Epigenetic Therapy for Non–Small Cell Lung Cancer
Authors: Patrick M. Forde, Julie R. Brahmer, Ronan J. Kelly
Journal: Clinical Cancer Research (2014)

Recent discoveries that non-small cell lung cancer (NSCLC) can be divided into molecular subtypes based on the presence or absence of driver mutations have revolutionized the treatment of many patients with advanced disease. However, despite these advances, a majority of patients are still dependent on modestly effective cytotoxic chemotherapy to provide disease control and prolonged survival. In this article, we review the current status of attempts to target the epigenome, heritable modifications of DNA, histones, and chromatin that may act to modulate gene expression independently of DNA coding alterations, in NSCLC and the potential for combinatorial and sequential treatment strategies.
LRRK2 Controls an EndoA Phosphorylation Cycle in Synaptic Endocytosis
Authors: Samer Matta, Kristof Van Kolen, Raquel da Cunha, Geert van den Bogaart, Wim Mandemakers, Katarzyna Miskiewicz, Pieter-Jan De Bock, Vanessa A. Morais, Sven Vilain, Dominik Haddad, Lore Delbroek, Jef Swerts, Lucía Chávez-Gutiérrez, Giovanni Esposito, Guy Daneels, Eric Karran, Matthew Holt, Kris Gevaert, Diederik W. Moechars, Bart De Strooper, Patrik Verstreken
Journal: Neuron (2012)
Does Allergen-Specific Immunotherapy Reduce the Risk, Reverse, and/or Mitigate Asthma in Children with Allergic Rhinitis? The Pediatric IMproved Access to AllerGen-Specific ImmuNothErapy - Asthma Incidence Rates Among Medicaid Enrollees (Pediatric-IMAGINE-AIRE) Study, Funded by the Joint Council of Allergy, Asthma and Immunology
Authors: C.S. Hankin, L. Cox, A. Bronstone, Z. Wang
Journal: Journal of Allergy and Clinical Immunology (2012)
p53 Genotypes and Haplotypes Associated With Lung Cancer Susceptibility and Ethnicity
Authors: X. Wu
Journal: JNCI Journal of the National Cancer Institute (2002)

Background: The p53 tumor suppressor protein is important in cell-cycle control, apoptosis, and DNA repair. Mutations in p53 have been associated with inherited cancer susceptibility. Because there is a difference in the risk of lung cancer among different ethnic groups, we examined associations between ethnicity and three polymorphisms in p53 (one exonic and two intronic) and haplotypes for the three loci and risk of lung cancer. We also examined the functionality of the p53 variants in apoptosis and DNA repair. Methods: In a case–control study, we frequency matched (by age, sex, and ethnicity) 635 lung cancer case patients and 635 control subjects. p53 genotypes and haplotypes at the three polymorphic sites were determined by restriction fragment length polymorphism analysis of lymphocyte DNA. Odds ratios (ORs) and 95% confidence intervals (CIs) for the association between genotype or haplotype and lung cancer risk were determined by logistic regression analysis. Apoptosis and DNA repair capacity were measured in 22 lymphoblastoid cell lines to determine the functional effects of the polymorphisms. All statistical tests were two-sided. Results: Genotype and haplotype frequency distributions were strongly dependent on ethnicity; variant allele frequencies were highest in African-Americans (29.1%) and lowest in Mexican-Americans (12.2%). Each of the three polymorphisms was associated with an increased risk of lung cancer among all ethnic groups. Moreover, for all three polymorphisms, increased variant allele copy number was associated with increased risk of lung cancer. Similarly, the variant haplotypes were also associated with an increased risk for lung cancer. Lymphoblastoid cell lines with all wild-type alleles at the three loci had statistically significantly higher apoptotic indices (13.66%, 95% CI = 8.61% to 18.71%) and DNA repair capacity (27.63%, 95% CI = 21.72% to 33.53%) than cell lines with at least one variant allele at all three loci (3.50%, 95% CI = 1.08% to 5.91%; and 17.48%, 95% CI = 7.99% to 26.96%, respectively). Conclusions: p53 polymorphisms may be associated with increased lung cancer risk and may affect p53 function.
Bowen's Disease as a Predictor of Malignancy
Authors: James Bryant
Journal: JAMA (1987)

To the Editor.—  In response to the article by Arbesman and Ransohoff1in the Jan 23/30,1987, issue ofJAMA, I would like to suggest a different approach to the problem of using Bowen's disease as a predictor of internal malignancy. Rather than attempting to pair Bowen's disease with future occurrences of all types of internal malignancy, more valid associations might be developed by pairing Bowen's disease with a specific internal malignancy. Cowden's disease, which includes multiple tricholemmomas among its physical signs, is associated with a high incidence of breast cancer.2Skin tags have been shown to serve as cutaneous markers for adenomatous polyps of the colon.3Bowen's disease may be associated with a particular internal malignancy in a highly predictive manner. The data generated over the past generation may not be totally useless, as the authors are suggesting, and could be reanalyzed, pairing Bowen's disease with the
Myenteric plexitis in enteric dysmotility: what are the implications for clinical practice?
Authors: J. E. Kellow
Journal: Gut (2009)

The term enteric dysmotility (ED) has been proposed1 to describe patients with recurrent severe gastrointestinal symptoms (nausea, vomiting, abdominal pain, abdominal distension, diarrhoea or constipation) and abnormal small bowel manometry, but without clinical or radiological evidence of previous or current mechanical bowel obstruction, occlusive episodes or bowel dilatation, and without evidence of any medication that could lead to small bowel motor abnormalities. The study in the current issue of Gut by Lindberg et al ( see page 1084 ) represents a potentially significant advance in our understanding of the pathophysiology of motility and functional gastrointestinal disorders (FGIDs), such as ED.2 The authors in this study examined, for the first time, full-thickness small bowel (usually jejunal) biopsies in 65 adult patients with the diagnosis of ED. These patients were found, using tangential sections, to exhibit a histological lesion classified as an inflammatory neuropathy—that is, neuron degeneration associated with an infiltration (mostly low grade) of CD3+ T lymphocytes in and around the ganglia of the myenteric plexus (and in some cases along axons). The prevalence of this inflammatory neuropathy was significantly greater in this group of patients with ED when compared with patients with chronic intestinal pseudo-obstruction who were also evaluated in this report.

The findings in this series extend and strengthen the validity of the findings in a previous report from the same investigators3 that described similar histological findings …
Cytokine gene polymorphisms in bullous pemphigoid in a Chinese population
Authors: Y.T. Chang, H.N. Liu, C.W. Yu, M.W. Lin, C.H. Huang, C.C. Chen, M.T. Liu, D.D. Lee, W.J. Wang, S.F. Tsai
Journal: British Journal of Dermatology (2005)

Journal Article Cytokine gene polymorphisms in bullous pemphigoid in a Chinese population Get access Y.T. Chang, Y.T. Chang Departments of DermatologyDepartment of Dermatology Dr Yun‐Ting Chang. E‐mail: ytchang@vghtpe.gov.tw Search for other works by this author on: Oxford Academic Google Scholar H.N. Liu, H.N. Liu Departments of DermatologyDepartment of DermatologyDepartment of Dermatology, National Defence Medical Centre, Taipei, Taiwan, Republic of China Search for other works by this author on: Oxford Academic Google Scholar C.W. Yu, C.W. Yu Departments of Dermatology Search for other works by this author on: Oxford Academic Google Scholar M.W. Lin, M.W. Lin Medical Research and Education, Taipei Veterans General Hospital, Shih‐Pai, Taipei 11217, Taiwan, Republic of ChinaFaculty of Medicine Search for other works by this author on: Oxford Academic Google Scholar C.H. Huang, C.H. Huang Departments of DermatologyDepartment of Dermatology Search for other works by this author on: Oxford Academic Google Scholar C.C. Chen, C.C. Chen Departments of DermatologyDepartment of Dermatology Search for other works by this author on: Oxford Academic Google Scholar M.T. Liu, M.T. Liu Departments of DermatologyDepartment of Dermatology Search for other works by this author on: Oxford Academic Google Scholar D.D. Lee, D.D. Lee Departments of DermatologyDepartment of Dermatology Search for other works by this author on: Oxford Academic Google Scholar W.J. Wang, W.J. Wang Departments of DermatologyDepartment of Dermatology Search for other works by this author on: Oxford Academic Google Scholar S.F. Tsai S.F. Tsai Institute of Genetics, National Yang‐Ming University, Taipei, Taiwan, Republic of ChinaDivision of Molecular & Genomic Medicine, National Health Research Institutes, Taipei, Taiwan, Republic of China Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 154, Issue 1, 1 January 2006, Pages 79–84, https://doi.org/10.1111/j.1365-2133.2005.06938.x Published: 01 January 2006 Article history Accepted: 20 May 2005 Published: 01 January 2006
Hypopituitarism and Diabetes
Authors: F. D. Hart
Journal: BMJ (1957)

<h3>ABSTRACT</h3> SARS-CoV-2 transmission risk generally increases with proximity of those shedding the virus to those susceptible to infection. Thus, this risk is a function of both number of people and the area which they occupy. However, the latter continues to evade COVID-19 testing policy. Increased testing in areas with lower population density, has the potential to induce a false sense of security even as cases continue to rise sharply overall.
Adenosine promotes neutrophil chemotaxis.
Authors: F R Rose, R Hirschhorn, G Weissmann, B N Cronstein
Journal: The Journal of Experimental Medicine (1988)

We have previously (1-4) demonstrated that adenosine, by engaging specific receptors on the surface of neutrophils, inhibits generation of toxic oxygen metabolites by activated neutrophils and prevents these activated neutrophils from injuring endothelial cells. We now report the surprising observation that engagement of these same neutrophil adenosine receptors promotes chemotaxis to C5 fragments (as zymosan-activated plasma [ZAP]) or to the bacterial chemoattractant FMLP. When chemotaxis was studied in a modified Boyden chamber, physiologic concentrations of adenosine promoted chemotaxis by as much as 60%. Adenosine receptor analogues, 5'N-ethylcarboxamidoadenosine (NECA) and N6-phenylisopropyladenosine (PIA), also promoted chemotaxis; the order of agonist potency was consistent with that of an A2 adenosine receptor (NECA greater than PIA greater than or equal to adenosine). A potent antagonist at adenosine receptors, 8-p-sulfophenyltheophylline (10 microM), completely reversed NECA enhancement of chemotaxis but did not affect chemotaxis by itself. Neither NECA nor 2-chloroadenosine, a nonselective adenosine receptor agonist, alone was chemotactic or chemokinetic by checkerboard analysis. NECA also promoted chemotaxis quantitated by a different technique, chemotaxis under agarose, to the surrogate bacterial chemoattractant FMLP. These data suggest that engagement of adenosine A2 receptors uniquely modulates neutrophil function so as to promote migration of neutrophils to sites of tissue damage while preventing the neutrophils from injuring healthy tissues en route.
Combined high-resolution array-based comparative genomic hybridization and expression profiling of ETV6/RUNX1-positive acute lymphoblastic leukemias reveal a high incidence of cryptic Xq duplications and identify several putative target genes within the commonly gained region
Authors: H Lilljebjörn, M Heidenblad, B Nilsson, C Lassen, A Horvat, J Heldrup, M Behrendtz, B Johansson, A Andersson, T Fioretos
Journal: Leukemia (2007)
Cognitive Behavior Therapy for Depression? Choose Horses for Courses
Authors: Gordon Parker, Kay Roy, Kerrie Eyers
Journal: American Journal of Psychiatry (2003)

OBJECTIVE: Although cognitive behavior therapy is a widely accepted treatment for depression, the problematic nature of efficacy studies is insufficiently recognized. METHOD: The authors reviewed original studies and quantitative analyses on the use of cognitive behavior therapy for depression. RESULTS: The authors suggested that claims for cognitive behavior therapy's efficacy on depression have been overstated, questioned whether its efficacy fits within its theoretical underpinning, and argued against viewing cognitive behavior therapy as a universal rather than a targeted strategy. CONCLUSIONS: Although cognitive behavior therapy may act more by its nonspecific therapeutic ingredients, the authors argued that by testing cognitive behavior therapy's efficacy in heterogeneous study groups, rather than in specific subgroups, failure to differentiate it from control therapies may have been ensured.
CORRECTION
Authors: M J Ledson, M J Walshaw
Journal: Thorax (2005)

We read with interest the paper by Jones et al 1 indicating the experience of the Manchester Adult CF Unit in the survival of patients with cystic fibrosis (CF) in the first 5 years following chronic infection with the B cepacia complex (Bcc).

The authors appear to have shown that 31 patients with B cenocepacia had a worse prognosis than Pseudomonas aeruginosa infected patients. Despite the title of the paper, they had insufficient patients chronically infected with B multivorans to draw any similar conclusions. Although these are not new findings, we congratulate them on their attempt to throw light on a difficult topic within the microbiology of CF. However, there are several anomalies in the study that cause concern. Firstly, they state that the 5 year survival in the B cenocepacia group was 66.6%, yet the figure (which incidentally contains data for 7 years) clearly shows the rate to be around 30%. Also, table 2 states that 19 (of 31) of these patients (61%) died within the study period, a value that fits with neither of the two …
Innate Immunity Derived Factors as External Modulators of the CXCL12 - CXCR4 Axis and Their Role in Stem Cell Homing and Mobilization
Authors: Mariusz Z. Ratajczak, Karol Serwin, Gabriela Schneider
Journal: Theranostics (2013)

The α-chemokine CXCL12 (stromal derived factor-1; SDF-1) and its corresponding G(αI) protein-coupled CXCR4 receptor axis play an important role in retention of hematopoietic stem progenitor cells (HSPCs) in bone marrow (BM) stem cell niches. CXCL12 has also been identified as a strong chemoattractant for HSPCs and implicated both in homing of HSPCs to BM after transplantation and in egress of these cells from BM into peripheral blood (PB). However, since CXCL12, as a peptide, is highly susceptible to degradation by proteolytic enzymes, its real biological availability in biological fluids may be somewhat limited. In this review, we will present data demonstrating that the CXCL12-CXCR4 axis is positively modulated by innate immunity-derived several external factors, ensuring that even low (near threshold) doses of CXCL12 still exert a robust chemotactic influence on HSPCs.