tbuckley/cabot-search huggingface dataset:
Regulatory Lymphocytes and Intestinal Inflammation
Authors: Ana Izcue, Janine L. Coombes, Fiona Powrie
Journal: Annual Review of Immunology (2009)

The immune system is pivotal in mediating the interactions between host and microbiota that shape the intestinal environment. Intestinal homeostasis arises from a highly dynamic balance between host protective immunity and regulatory mechanisms. This regulation is achieved by a number of cell populations acting through a set of shared regulatory pathways. In this review, we summarize the main lymphocyte subsets controlling immune responsiveness in the gut and their mechanisms of control, which involve maintenance of intestinal barrier function and suppression of chronic inflammation. CD4 + Foxp3 + T cells play a nonredundant role in the maintenance of intestinal homeostasis through IL-10- and TGF-β-dependent mechanisms. Their activity is complemented by other T and B lymphocytes. Because breakdown in immune regulatory networks in the intestine leads to chronic inflammatory diseases of the gut, such as inflammatory bowel disease and celiac disease, regulatory lymphocytes are an attractive target for therapies of intestinal inflammation.
BioWardrobe: an integrated platform for analysis of epigenomics and transcriptomics data
Authors: Andrey V. Kartashov, Artem Barski
Journal: Genome biology (2015)

High-throughput sequencing has revolutionized biology by enhancing our ability to perform genome-wide studies. However, due to lack of bioinformatics expertise, modern technologies are still beyond the capabilities of many laboratories. Herein, we present the BioWardrobe platform, which allows users to store, visualize and analyze epigenomics and transcriptomics data using a biologist-friendly web interface, without the need for programming expertise. Predefined pipelines allow users to download data, visualize results on a genome browser, calculate RPKMs (reads per kilobase per million) and identify peaks. Advanced capabilities include differential gene expression and binding analysis, and creation of average tag -density profiles and heatmaps. BioWardrobe can be found at http://biowardrobe.com .
Heightened bronchial hyperresponsiveness in the absence of heightened atopy in children with current wheezing and low-income status.
Authors: Javier Mallol, Jose A. Castro-Rodriguez, Eliana Cortez, Viviana Aguirre, Pedro Aguilar, Barrueto Luis
Journal: Thorax (2007)

Background : Although global studies as ISAAC have provided with valuable data on the prevalence of asthma in children of Latin America, there is very few information on the relationship between asthma symptoms, pulmonary function, bronchial hyperresponsiveness and atopy in the region. Methods: This study examined the relationship between self-reported wheezing in the last 12 months, pulmonary function, airway responsiveness and atopy in children from a low-income population neighborhood in Santiago, Chile. Two random samples (100 each) of children aged 13-14 years who participated in ISAAC Phase One were selected according to whether they have reported or not, wheezing in the last 12 months. Spirometry, methacholine bronchial challenge test and prick test were performed in all individuals. Results: Children who reported current wheezing had significantly higher bronchial hyperresponsiveness (BHR) to methacholine as compared to those without wheezing (71.6% vs.52.6%, respectively; p=0.007,) and no significant difference was found in FEV1 (116.7„b12.3% vs. 120.3„b14.5%, respectively, p=0.11). The prevalence of atopy was not significantly different between those children who reported wheezing as compared to those who did not (44.2% vs. 42.3%; respectively, p=0.89). Multiple regression analysis showed that only BHR to methacholine (OR 2.72, 95% CI: 1.25-4.13, p=0.01) and maternal asthma (OR 3.1, 95%CI 1.2-8.3, p=0.03) were significant risk factors for current wheezing. Conclusions: Our results support previous findings suggesting that in adolescents from unprivileged populations, self-reported current wheezing is related to BHR but not to atopy.
UNION AND NON-UNION OF FRACTURES
Authors: A. S. B. Bankart
Journal: BMJ (1930)

she had not got malignant disease of the uterus, it would relieve thousands of women of a haunitinig fear.Con- versely, they should be told that if they have a lump in the breast they must at once consult a doctor, anid likewise if they have any irregular haemorrlrage.When, however, such propaganda is sent out it should also he explailned that lnot every lump in the breast is cancer, and that a gireat many cases of irri-egular halemorirhage are niot duc to this seriiou-s conditioni.
Effects of Barbiturates on Pulmonary and Systemic Haemodynamics
Authors: S. J. Goldberg, L. M. Linde, P. G. Gaal, K. Momma, M. Takahashi, G. Sarna
Journal: Cardiovascular Research (1968)

Journal Article Effects of Barbiturates on Pulmonary and Systemic Haemodynamics Get access Stanley J. Goldberg, Stanley J. Goldberg From the Division of Cardiology, Department of Pediatrics and Department of Surgery, UCLA School of Medicine, Los Angeles, California, U.S.A. Search for other works by this author on: Oxford Academic PubMed Google Scholar Leonard M. Linde, Leonard M. Linde From the Division of Cardiology, Department of Pediatrics and Department of Surgery, UCLA School of Medicine, Los Angeles, California, U.S.A. Search for other works by this author on: Oxford Academic PubMed Google Scholar Peter G. Gaal, Peter G. Gaal From the Division of Cardiology, Department of Pediatrics and Department of Surgery, UCLA School of Medicine, Los Angeles, California, U.S.A. Search for other works by this author on: Oxford Academic PubMed Google Scholar Kazuo Momma, Kazuo Momma From the Division of Cardiology, Department of Pediatrics and Department of Surgery, UCLA School of Medicine, Los Angeles, California, U.S.A. Search for other works by this author on: Oxford Academic PubMed Google Scholar Masato Takahashi, Masato Takahashi From the Division of Cardiology, Department of Pediatrics and Department of Surgery, UCLA School of Medicine, Los Angeles, California, U.S.A. Search for other works by this author on: Oxford Academic PubMed Google Scholar Gregory Sarna Gregory Sarna From the Division of Cardiology, Department of Pediatrics and Department of Surgery, UCLA School of Medicine, Los Angeles, California, U.S.A. Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 2, Issue 2, April 1968, Pages 136–142, https://doi.org/10.1093/cvr/2.2.136 Published: 01 April 1968 Article history Received: 25 September 1967 Published: 01 April 1968
Following Cytochrome <i>c</i> Release, Autophagy Is Inhibited during Chemotherapy-Induced Apoptosis by Caspase 8–Mediated Cleavage of Beclin 1
Authors: Hua Li, Peng Wang, Quanhong Sun, Wen-Xing Ding, Xiao-Ming Yin, Robert W. Sobol, Donna B. Stolz, Jian Yu, Lin Zhang
Journal: Cancer Research (2011)

Abstract Autophagy is an evolutionarily conserved stress response mechanism that often occurs in apoptosis-defective cancer cells and can protect against cell death. In this study, we investigated how apoptosis and autophagy affect each other in cancer cells in response to chemotherapeutic treatment. We found that specific ablation of the proapoptotic function of cytochrome c, a key regulator of mitochondria-mediated apoptosis, enhanced autophagy following chemotherapeutic treatment. Induction of autophagy required Beclin 1 and was associated with blockage of Beclin 1 cleavage by caspase 8 at two sites. To investigate the role of Beclin 1 cleavage in the suppression of autophagy and cell survival, a caspase-resistant mutant of Beclin 1 was knocked into HCT116 colon cancer cells. Beclin 1 mutant knockin resulted in markedly increased autophagy and improved long-term cell survival after chemotherapeutic treatment but without affecting apoptosis and caspase activation. Furthermore, Beclin 1 mutant tumors were significantly less responsive to chemotherapeutic treatment than were wild-type tumors. These results show that chemotherapy-induced apoptosis inhibits autophagy at the execution stage subsequent to cytochrome c release through caspase 8–mediated cleavage of Beclin 1. If apoptosis fails to execute, autophagy is unleashed due to lack of Beclin 1 cleavage by caspases and can contribute to cancer cell survival and therapeutic resistance. Therefore, Beclin 1 may be a useful target for inhibiting autophagy to sensitize chemotherapy. Cancer Res; 71(10); 3625–34. ©2011 AACR.
Lamivudine and alpha interferon combination therapy in patients with anti-HBE-positive chronic hepatitis B: preliminary results of a randomised study
Authors: S. Kaymakoglu, K. Demir, Y. Cakaloglu, Z. Durakoglu, D. Dincer, C. Karaca, H. Umit, S. Turkoglu, S. Badur, F. Besisik, A. Okten
Journal: Journal of Hepatology (2001)
Acute nonlymphocytic leukemia (M7 subtype) with erythrocytic internalization
Authors: S. Woessner, R. Lafuente, M. Giralt, J. Molina, L. Florensa
Journal: American Journal of Hematology (1986)

Abstract A case of acute nonlymphocytic leukemia of megakaryocytic lineage or M7 with a conspicuous phenomenon of erythrocytic internalization present in nearly 3% of the leukemic megakaryocytic precursors (LMP) is reported. The phagocytosis was detected at light microscopy and ultrastructural levels. The erythrocyte might have reached the interior of the LMP through cytoplasmic vacuoles that are connected with the extracellular space and that can be considered rudimentary equivalents of the demarcation membrane system (DMS). Erythrocytic internalization is not a specific feature of the mononuclear phagocytic system and can be misleading in the classification of undifferentiated blast cells.
American Society of Clinical Oncology 2009 Clinical Evidence Review on Radiofrequency Ablation of Hepatic Metastases From Colorectal Cancer
Authors: Sandra L. Wong, Pamela B. Mangu, Michael A. Choti, Todd S. Crocenzi, Gerald D. Dodd, Gary S. Dorfman, Cathy Eng, Yuman Fong, Andrew F. Giusti, David Lu, Thomas A. Marsland, Rob Michelson, Graeme J. Poston, Deborah Schrag, Jerome Seidenfeld, Al B. Benson
Journal: Journal of Clinical Oncology (2009)

Purpose To review the evidence about the efficacy and utility of radiofrequency ablation (RFA) for hepatic metastases from colorectal cancer (CRHM). Methods The American Society of Clinical Oncology (ASCO) convened a panel to conduct and analyze a comprehensive systematic review of the RFA literature from Medline and the Cochrane Collaboration Library. Results Because data were considered insufficient to form the basis of a practice guideline, ASCO has instead published a clinical evidence review. The evidence is from single-arm, retrospective, and prospective trials. No randomized controlled trials have been included. The following three clinical issues were considered by the panel: the efficacy of surgical hepatic resection versus RFA for resectable tumors; the utility of RFA for unresectable tumors; and RFA approaches (open, laparoscopic, or percutaneous). Evidence suggests that hepatic resection improves overall survival (OS), particularly for patients with resectable tumors without extrahepatic disease. Careful patient and tumor selection is discussed at length in the literature. RFA investigators report a wide variability in the 5-year survival rate (14% to 55%) and local tumor recurrence rate (3.6% to 60%). The reported mortality rate was low (0% to 2%), and the major complications rate was commonly reported to be between 6% and 9%. RFA is currently performed with all three approaches. Conclusion There is a compelling need for more research to determine the efficacy and utility of RFA to increase local recurrence-free, progression-free, and disease-free survival as well as OS for patients with CRHM. Clinical trials have established that hepatic resection can improve OS for patients with resectable CRHM.
Accelerated Telomere Shortening Precedes Development of Therapy-Related Myelodysplasia or Acute Myelogenous Leukemia After Autologous Transplantation for Lymphoma
Authors: Sujata Chakraborty, Can-Lan Sun, Liton Francisco, Melanie Sabado, Liang Li, Karen L. Chang, Stephen Forman, Smita Bhatia, Ravi Bhatia
Journal: Journal of Clinical Oncology (2009)

Purpose Therapy-related myelodysplasia or acute myelogenous leukemia (t-MDS/AML) is a lethal complication of autologous hematopoietic stem-cell transplantation (aHCT) for Hodgkin's lymphoma (HL) and non-Hodgkin's lymphoma (NHL). Here, we investigated the hypothesis that accelerated telomere shortening after aHCT could contribute to the development of t-MDS/AML. Patients and Methods A prospective longitudinal cohort was constructed to investigate the sequence of cellular and molecular abnormalities leading to development of t-MDS/AML after aHCT for HL/NHL. This cohort formed the sampling frame for a nested case-control study to compare changes in telomere length in serial blood samples from patients who developed t-MDS/AML with matched controls who did not develop t-MDS/AML. Results An initial increase in telomere length at day 100 after aHCT was followed by an accelerated telomere shortening in t-MDS/AML patients when compared with controls. These telomere alterations preceded the onset of t-MDS and were independent of other known risk factors associated with development of t-MDS/AML on multivariate analysis. Additionally, we observed reduced generation of committed progenitors in patients who developed t-MDS/AML, indicating that these telomere alterations were associated with reduced regenerative capacity of hematopoietic stem cells. Conclusion The development of t-MDS/AML after aHCT is associated with and preceded by markedly altered telomere dynamics in hematopoietic cells. Accelerated telomere loss in patients developing t-MDS/AML may reflect increased clonal proliferation and/or altered telomere regulation in premalignant cells. Genetic instability associated with shortened telomeres may contribute to leukemic transformation in t-MDS/AML.
Comparison of the Forced Oscillation Technique and the Interrupter Technique for Assessing Airway Obstruction and Its Reversibility in Children
Authors: CHRISTOPHE DELACOURT, HUBERT LORINO, CLAIRE FUHRMAN, MARTINE HERVE-GUILLOT, PHILIPPE REINERT, ALAIN HARF, BRUNO HOUSSET
Journal: American Journal of Respiratory and Critical Care Medicine (2001)

The forced oscillation technique (FOT) and interrupter technique are particularly attractive for pediatric use as they require only passive cooperation from the patient. We compared the sensitivity and specificity of these methods for detecting airway obstruction and its reversibility in 118 children (3–16 yr) with asthma or chronic nocturnal cough. FOT (R0 and R16) and interruption (Rint) parameters were measured at baseline and after bronchodilator inhalation (n = 94). Rint was significantly lower than R0, especially in children with high baseline values. Baseline parameters were normalized for height and weight [R(SD)]. In children able to perform forced expiratory maneuvers (n = 93), the best discrimination between those with baseline FEV1 < 80% or ⩾ 80% of predicted values was obtained with R0(SD). At a specificity of 80%, R0(SD) yielded 66% sensitivity, whereas Rint(SD) yielded only 33% sensitivity. Similarly, postbronchodilator changes in R0(SD) [ Δ R0(SD)] yielded the best discrimination between children with and without significant reversibility in FEV1. At a specificity of 80%, Δ R0(SD) yielded 67% sensitivity and Δ Rint(SD) yielded 58% sensitivity. In children unable to perform forced expiratory maneuvers (n = 25), FOT, contrary to the interrupter technique, clearly identified a subgroup of young children with high resistance values at baseline, which returned to normal after bronchodilation. We conclude that, in asthmatic children over 3 yr old, FOT measurements provide a more reliable evaluation of bronchial obstruction and its reversibility compared with the interrupter technique, especially in young children with high baseline values.
Response to Letter Regarding Article, “Metabolic Profiling of Arginine and Nitric Oxide Pathways Predicts Hemodynamic Abnormalities and Mortality in Patients With Cardiogenic Shock After Acute Myocardial Infarct”
Authors: Stephen J. Nicholls, Steven E. Nissen, Stanley L. Hazen, Zeneng Wang, Robert Koeth, Bruce Levison, Brian DelFraino, Vladimir Dzavik, Owen W. Griffith, David Hathaway, Julio A. Panza, Judith S. Hochman
Journal: Circulation (2008)
Mechanism of Effect of Hypoxia on Renal Water Excretion
Authors: Robert J. Anderson, Richard G. Pluss, Arnold S. Berns, James T. Jackson, Patricia E. Arnold, Robert W. Schrier, Keith M. McDonald
Journal: Journal of Clinical Investigation (1978)

The effect of lowering the pressure of oxygen from 80 to 34 mm Hg was examined in anesthetized dogs that were undergoing a water diuresis. This degree of hypoxia was associated with an antidiuresis as urine osmolality (Uosm) increased from 107 to 316 mosmol/kg H2O (P < 0.001) and plasma arginine vasopressin increased from 0.06 to 7.5 μU/ml, (P < 0.05). However, hypoxia was not associated with significant changes in cardiac output (CO, from 4.2 to 4.7 liters/ min), mean arterial pressure (MAP, from 143 to 149 mm Hg), glomerular filtration rate (GFR, from 46 to 42 ml/min), solute excretion rate (SV, from 302 to 297 mosmol/min), or filtration fraction (from 0.26 to 0.27, NS). Hypoxia was associated with an increase in renal vascular resistance (from 0.49 to 0.58 mm Hg/ml per min, P < 0.01). The magnitude of hypoxia-induced antidiuresis was the same in innervated kidneys and denervated kidneys. To further examine the role of vasopressin in this antidiuresis, hypoxia was induced in hypophysectomized animals. The effect of hypoxia on CO, MAP, GFR, SV, and renal blood flow in hypophysectomized animals was the same as in intact animals. In contrast to intact animals, however, hypoxia did not induce a significant antidiuresis in hypophysectomized animals (Uosm from 72 to 82 mosmol/kg H2O). To delineate the afferent pathway for hypoxia-stimulated vasopressin release, hypoxia was induced in dogs with either chemo- or baroreceptor denervation. The effect of hypoxia on CO, MAP, GFR, SV, and renal blood flow in the denervated animals was the same as in nondenervated animals. Hypoxia resulted in an antidiuresis in chemoreceptor (Uosm from 113 to 357 mosmol/kg H2O, P < 0.001) but not in baroreceptor (Uosm from 116 to 138 mosmol/kg H2O, NS) denervated animals. To determine if hypoxia alters renal response to vasopressin, exogenous vasopressin was administered to normoxic and hypoxic groups of dogs. The antidiuretic effect of vasopressin was no different in these two groups. These results demonstrate that hypoxia induces an antidiuresis which is independent of alterations in CO, MAP, SV, filtration fraction, renal nerves, or renal response to vasopressin and occurs through baroreceptor-mediated vasopressin release. The nature of the baroreceptor stimulation remains to be elucidated.
Regulation of Tumor Invasion by Cartilage-Derived Anti-Invasion Factor In Vitro&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;&lt;xref ref-type="fn" rid="FN3"&gt;3&lt;/xref&gt;
Authors: B U Pauli, V A Memoli, K E Kuettner
Journal: JNCI Journal of the National Cancer Institute (1981)

The resistance of cartilage to tumor invasion was studied with the use of a novel in vitro culture system. Articular cartilage obtained from fresh metacarpophalangeal joints of preadolescent bovines was used as a growth surface for human TE-85 osteosarcoma cells and foreskin fibroblasts. Cartilage disks formed the bottoms of stainless-steel cylinders, providing closed growth chambers for these cells. Both invasive osteosarcoma cells and normal fibroblasts were unable to penetrate viable, unextracted cartilage during a 2-week culture period. When cartilage was devitalized by freezing and thawing, the tissue remained resistant to invasion. Cartilage, extracted with either 1 or 3 M guanidine hydrochloride, was invaded by osteosarcoma cells, but not by control fibroblasts. Invasion by osteosarcoma cells into salt-extracted cartilage was abolished when low concentrations of a cartilage-derived, anti-invasion factor were added to the culture medium. These data provided evidence that the resistance of cartilage to tumor invasion is regulated in part by tissue-derived proteinase inhibitors.
Oxidative stress causes enhanced endothelial cell injury in human heme oxygenase-1 deficiency
Authors: Akihiro Yachie, Yo Niida, Taizo Wada, Noboru Igarashi, Hisashi Kaneda, Tomoko Toma, Kazuhide Ohta, Yoshihito Kasahara, Shoichi Koizumi
Journal: Journal of Clinical Investigation (1999)

The first known human case of heme oxygenase-1 (HO-1) deficiency is presented in this report. The patient is a six-year-old boy with severe growth retardation. He has been suffering from persistent hemolytic anemia characterized by marked erythrocyte fragmentation and intravascular hemolysis, with paradoxical increase of serum haptoglobin and low bilirubin. An abnormal coagulation/fibrinolysis system, associated with elevated thrombomodulin and von Willebrand factor, indicated the presence of severe, persistent endothelial damage. Electron microscopy of renal glomeruli revealed detachment of endothelium, with subendothelial deposition of an unidentified material. Iron deposition was noted in renal and hepatic tissue. Immunohistochemistry of hepatic tissue and immunoblotting of a cadmium-stimulated Epstein-Barr virus–transformed lymphoblastoid cell line (LCL) revealed complete absence of HO-1 production. An LCL derived from the patient was extremely sensitive to hemin-induced cell injury. Sequence analysis of the patient's HO-1 gene revealed complete loss of exon-2 of the maternal allele and a two-nucleotide deletion within exon3 of the paternal allele. Growth retardation, anemia, iron deposition, and vulnerability to stressful injury are all characteristics observed in recently described HO–1 targeted mice. This study presents not only the first human case of HO-1 deficiency but may also provide clues to the key roles played by this important enzyme in vivo.