tbuckley/cabot-search huggingface dataset:
Human Fibroblast Interferon and Acyclovir in Cytomegalovirus Pneumonia
Authors: M. J. Gill, J. Russel, K. Burgess, Y. H. Tan
Journal: Annals of Internal Medicine (1986)

Letters and Corrections1 January 1986Human Fibroblast Interferon and Acyclovir in Cytomegalovirus PneumoniaM. J. GILL, M.B., F.R.C.P.(C), J. RUSSEL, M.B., F.R.C.P.(UK), K. BURGESS, M.B., F.R.C.P.(C), Y. H. TAN, Ph.D.M. J. GILL, M.B., F.R.C.P.(C)Search for more papers by this author, J. RUSSEL, M.B., F.R.C.P.(UK)Search for more papers by this author, K. BURGESS, M.B., F.R.C.P.(C)Search for more papers by this author, Y. H. TAN, Ph.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-104-1-129_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The recent study of Shepp and colleagues (1) highlights the complex and serious nature of cytomegalovirus pneumonitis occurring in bone marrow transplant recipients. Nine of their ten patients died of the pneumonitis, despite the significant effect of their new antiviral agent on the cytomegalovirus infection. Their study shows the overall disease progressing despite the potent activity of the chemical antiviral agent against the presumed pathogen. In the past, acyclovir, vidarabine, and leukocyte (alpha) interferon, either alone or in combinations, have also proved ineffective in improving survival rates. Recently hyperimmune globulin has shown some promise in the therapy...References1. SHEPPDANDLIKERDE MIRANDA DPP. Activity of 9- [2-hydroxy-1-(hydroxymethyl)ethoxymethyl]guanine in the treatment of cytomegalovirus pneumonia. Ann Intern Med. 1985;103:368-73. LinkGoogle Scholar2. BLACKLOCKGRIFFITHSSTIRKPRENTICE HPPH. Specific hyperimmune globulin for cytomegalovirus pneumonitis. Lancet. 1985;2:152-3. CrossrefMedlineGoogle Scholar3. SPECTORTYNDALLKELLEY SME. Effects of acyclovir combined with other antiviral agents on human cytomegalovirus. Am J Med. 1982;73(1A):36-9. CrossrefMedlineGoogle Scholar4. EINHORNSTRANDER SH. Is interferon tissue specific? Effect of human leukocyte and fibroblast interferons on the growth of lymphoblastoid and osteosarcoma cell lines. J Gen Virol. 1977;35:573-7. CrossrefMedlineGoogle Scholar5. TANBARAKATBERTHOLDSMITH-JOHANNSENTAN YFWHC. The isolation and amino acid/sugar composition of human fibroblastoid interferon. J Biol Chem. 1979;254:8067-73. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByTherapy and Prevention of Cytomegalovirus Infections 1 January 1986Volume 104, Issue 1Page: 129-130KeywordsAntiviralsBone marrowCytomegalovirus infectionFibroblastsGlobulinsInterferonsPathogensPneumoniaPneumonitis Issue Published: 1 January 1986 PDF DownloadLoading ...
Diagnostic value of HSP70, glypican 3, and glutamine synthetase in hepatocellular nodules in cirrhosis
Authors: Luca Di Tommaso, Giada Franchi, Young Nyun Park, Barbara Fiamengo, Annarita Destro, Emanuela Morenghi, Marco Montorsi, Guido Torzilli, Maurizio Tommasini, Luigi Terracciano, Luigi Tornillo, Raffaella Vecchione, Massimo Roncalli
Journal: Hepatology (2007)

Abstract Hepatocellular nodules in cirrhosis include regenerative (large regenerative, LRN) and dysplastic (low and high grade, LGDN and HGDN) nodules, early and grade 1 HCC (eHCC-G1), and overt HCC. The differential diagnosis may be particularly difficult when lesions such as HGDN and eHCC-G1 are involved. We investigated the diagnostic yield of a panel of 3 putative markers of hepatocellular malignancy such as HSP70, glypican 3 (GPC3), and glutamine synthetase (GS). We selected 52 surgically removed nonmalignant nodules (15 LRNs, 15 LGDNs, 22 HGDNs) and 53 HCCs (10 early, 22 grade 1, and 21 grade 2-3) and immunostained them for HSP70, GPC3, and GS. The sensitivity and specificity of the individual markers for the detection of eHCC-G1 were 59% and 86% for GS, 69% and 91% for GPC3, and 78% and 95% for HSP70. We identified 2 main phenotypes: (1) all negative, seen in 100% LRN and LGDN, 73% HGDN and 3% eHCC-G1; (2) all positive, a feature detected in less than half the eHCC-G1. Using a 3-marker panel, when at least 2 of them, regardless which, were positive, the sensitivity and specificity for the detection of eHCC-G1 were respectively 72% and 100%; the most sensitive combination was HSP70+/GPC3+ (59%) when a 2-marker panel was used. Conclusion: The adopted panel of 3 markers is very helpful in distinguishing eHCC-G1 from dysplastic nodules arising in cirrhosis. (Hepatology 2007;45:725–734.)
Febrile and gynaecological infections in pregnancy increase the risk of childhood respiratory disorders in the offspring
Authors: Giancarlo Pesce, Alessandro Marcon, Pierpaolo Marchetti, Paolo Girardi, Roberto de Marco
Journal: European Respiratory Journal (2013)

Emerging evidence suggests that foetal and early life environmental factors are critical for determining the susceptibility to allergic and respiratory diseases. In the present study, we investigated whether maternal febrile infections (FI) or gynaecological infections (GI) during pregnancy are associated with allergic respiratory diseases in the offspring, and whether specific pregnancy trimesters are involved.  We enrolled 4,577 children, aged 3-14yr. Their parents filled in a standardized questionnaire about children’s respiratory health and the events occurred during pregnancy and at birth. We evaluated the incidence of wheezing, asthma and rhinitis, and the occurrence of five respiratory symptoms in the last 12 months.  Children born to mothers who reported FI and GI had more respiratory symptoms in the last 12 months (IRR:1.40, 95%CI:1.12-1.74 and IRR:1.60, 95%CI:1.24-2.06, respectively). This association was stronger when FI occurred in the 1st trimester of pregnancy (IRR:2.12, 95%CI:1.37-3.28).  The incidence of asthma was significantly higher in the children whose mothers reported FI or GI in the 1st trimester of pregnancy (HR:2.61, 95%CI:1.01-6.76 and HR:3.50, 95%CI:1.24-9.91, respectively). GI in the 3rd trimester were associated with higher risk of wheezing (HR:1.55, 95%CI:1.11-2.17) and rhinitis (HR:1.82; 95%CI:1.02-3.26).  FI and GI might increase the risk of developing respiratory symptoms and diseases, especially when occurring in specific trimesters of pregnancy. These findings suggest that FI and GI might interfere with foetal programming of respiratory and immune system through different mechanisms.
Mantle-Cell Lymphoma (Multiple Lymphomatous Polyposis) of the Entire GI Tract
Authors: Spyros Michopoulos, Kalliopi Petraki, Charis Matsouka, Efstathios Kastritis, Heleni Chrysanthopoulou, Meletios Athanasios Dimopoulos
Journal: Journal of Clinical Oncology (2008)
Desloratadine in combination with montelukast suppresses the dermographometer challenge test papule, and is effective in the treatment of delayed pressure urticaria: a randomized, double-blind, placebo-controlled study
Authors: E. Nettis, M.C. Colanardi, A.L. Soccio, A. Ferrannini, A. Vacca
Journal: British Journal of Dermatology (2006)

Journal Article Desloratadine in combination with montelukast suppresses the dermographometer challenge test papule, and is effective in the treatment of delayed pressure urticaria: a randomized, double‐blind, placebo‐controlled study Get access E. Nettis, E. Nettis Department of Medical Clinic, Immunology and Infectious Diseases, Division of Allergy and Clinical Immunology, andDepartment of Internal Medicine and Clinical Oncology, University of Bari Medical School, I‐70124 Bari, Italy Eustachio Nettis. E‐mail: e.nettis@allergy.uniba.it Search for other works by this author on: Oxford Academic Google Scholar M.C. Colanardi, M.C. Colanardi Department of Medical Clinic, Immunology and Infectious Diseases, Division of Allergy and Clinical Immunology, andDepartment of Internal Medicine and Clinical Oncology, University of Bari Medical School, I‐70124 Bari, Italy Search for other works by this author on: Oxford Academic Google Scholar A.L. Soccio, A.L. Soccio Department of Medical Clinic, Immunology and Infectious Diseases, Division of Allergy and Clinical Immunology, andDepartment of Internal Medicine and Clinical Oncology, University of Bari Medical School, I‐70124 Bari, Italy Search for other works by this author on: Oxford Academic Google Scholar A. Ferrannini, A. Ferrannini Department of Medical Clinic, Immunology and Infectious Diseases, Division of Allergy and Clinical Immunology, andDepartment of Internal Medicine and Clinical Oncology, University of Bari Medical School, I‐70124 Bari, Italy Search for other works by this author on: Oxford Academic Google Scholar A. Vacca A. Vacca Department of Medical Clinic, Immunology and Infectious Diseases, Division of Allergy and Clinical Immunology, andDepartment of Internal Medicine and Clinical Oncology, University of Bari Medical School, I‐70124 Bari, Italy Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 155, Issue 6, 1 December 2006, Pages 1279–1282, https://doi.org/10.1111/j.1365-2133.2006.07533.x Published: 01 December 2006 Article history Accepted: 09 June 2006 Published: 01 December 2006
Acute bronchiolitis in infancy: treatment and prognosis.
Authors: A D Milner, M Murray
Journal: Thorax (1989)

Acute bronchiolitis in infancy: treatment and prognosisAcute bronchiolitis is the most common severe lower respiratory tract infection of infancy.About 2% of all babies born in the previous 12 months will be admitted on July 20, 2023 by guest.
Measure Once or Twice Does It Really Matter?
Authors: S. G. Hilsenbeck, D. D. V. Hoff
Journal: JNCI Journal of the National Cancer Institute (1999)

There is an old carpenter’s dictum that one should measure twice (and cut once). Supposedly, this leads to fewer irreversible errors—with wood. The question is, do we have to measure a tumor twice in the practice of medical oncology? In an article in this issue of the Journal, James et al. (1) conclude that a one-dimensional measurement of tumor maximum diameter (rather than a two-dimensional measurement) may be sufficient to assess the change in solid tumors following treatment. The authors are to be congratulated for taking a new look at the “conventional wisdom” of the way we measure tumors. The question one must ask is, are there any reasons for the general practice of oncology to adopt unidimensional measurement of tumors? It is true, as pointed out by James et al. (1), that the process of measurement of tumors in two dimensions and the calculation of products and their sum is laborious. Anything that gives us more time to spend talking with our patients rather than measuring with calipers and calculating with a calculator is certainly welcome. However, one must remember that, to ascertain the maximum diameter of a tumor (since a tumor is frequently not exactly spherical), one usually takes more than one measurement to make sure one has the maximum diameter. Therefore, one may not save much time. On the positive side, requiring only unidimensionally measurable disease as an entry criterion (rather than the usually required bidimensionally measurable disease) may allow more patients to participate in clinical trials. However, allowing that there may be a savings of time by measuring each tumor in one dimension and having a larger percentage of patients able to participate in clinical trials, are there other reasons to adopt the unidimensional method? The authors present a theoretical reason for using only one dimension for measurement of tumor response. They posit that changes in diameter relate more closely to the fixed properties of cells killed by a standard dose of chemotherapy than do changes in the bidimensional product. However, we have some concerns about that reasoning. Assuming for the moment that we have a single, spherical tumor, then
Abnormalities of lipid metabolism in hepatitis C virus infection
Authors: F. Negro
Journal: Gut (2010)

The purpose of this study was to evaluate the usefulness of limited-flip-angle, phase-sensitive velocity imaging with gradient-recalled-echo (VIGRE) MR when combined with spin-echo MR in the diagnosis of dural sinus thrombosis. The VIGRE sequence consists of a rapid single-slice acquisition, 50/15/2 (TR/TE/excitations), and 30 degrees flip angle. At each slice position, a total of four images were reconstructed; these consisted of one magnitude image and three images sensitive to proton motion in each orthogonal direction. The flow direction and flow velocity (cm/sec) were obtained from each of the phase images, and results were correlated with data obtained from a phantom experiment. In normal controls, dural sinus velocities ranged from a mean of 9.9 to 14.4 cm/sec for the transverse and superior sagittal sinuses, respectively. Three patients with proved dural sinus occlusion were studied with spin-echo images at 1.5 T. Three-dimensional time-of-flight MR angiography was also performed in one patient. The presence of dural sinus occlusion was determined by the lack of flow void on the spin-echo images, the absence of phase shift on the VIGRE study, and the presence of retrograde flow on the phase image in the sinus proximal to the occluded segment. Time-of-flight angiography overestimated the extent of the thrombosis caused by spin saturation. Follow-up VIGRE studies detected the formation of collateral flow in one patient and recanalization with the establishment of normal antegrade sinus flow in the other. We conclude that phase-sensitive MR imaging is helpful in establishing the diagnosis and extent of dural sinus occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Effect of mitoxantrone on outcome of children with first relapse of acute lymphoblastic leukaemia (ALL R3): an open-label randomised trial
Authors: Catriona Parker, Rachel Waters, Carly Leighton, Jeremy Hancock, Rosemary Sutton, Anthony V Moorman, Philip Ancliff, Mary Morgan, Ashish Masurekar, Nicholas Goulden, Nina Green, Tamas Révész, Philip Darbyshire, Sharon Love, Vaskar Saha
Journal: The Lancet (2010)
Management of Pulmonary Disease in Patients with Cystic Fibrosis
Authors: Bonnie W. Ramsey
Journal: New England Journal of Medicine (1996)

Cystic fibrosis is the most common life-shortening autosomal recessive disorder in the white population, affecting approximately 30,000 persons in the United States.1 It is caused by mutations in a single gene on the long arm of chromosome 7 that encodes the cystic fibrosis transmembrane conductance regulator (CFTR) (Figure 1).2 CFTR has multiple functions involving fluid balance across epithelial cells. It acts as a chloride channel activated by cyclic adenosine monophosphate (cAMP)3 and may stimulate other chloride channels4 and inhibit sodium absorption by epithelial sodium channels.5 Mutations in the CFTR gene result in defective chloride transport in the epithelial cells in . . .
Generation of T cell colonies from responder strain 2 guinea pigs that recognize the copolymer L-glutamic acid, L-lysine in association with nonresponder strain 13 Ia antigens.
Authors: R B Clark, E M Shevach
Journal: The Journal of Experimental Medicine (1982)

T cells from nonimmune responder strain 2 guinea pigs were primed in vitro to the copolymer GL in association with allogeneic, nonresponder strain 13 PEC. T cells that recognized GL in association with strain 13 Ia were separated from alloreactive T cells by cloning the population in soft agar following the priming in liquid culture. The existence of T cells of responder origin that recognize antigen in association with nonresponder macrophages is most consistent with clonal deletion models of Ir gene function.
Effect of salmeterol compared with beclomethasone on allergen-induced asthmatic and inflammatory responses
Authors: MM Pizzichini, JC Kidney, BJ Wong, MM Morris, A Efthimiadis, J Dolovich, FE Hargreave
Journal: European Respiratory Journal (1996)

Salmeterol is a selective long-acting beta 2-agonist bronchodilator considered to have added anti-inflammatory effects, but this is controversial. We investigated the effects of a single dose of salmeterol, 100 micrograms, on the physiological and inflammatory responses to inhaled allergen and compared these with the effects of a single dose of beclomethasone, 500 micrograms, and of placebo. Eight atopic adults with mild stable asthma, treated only with inhaled short-acting beta 2-agonist when needed, attended the laboratory sequentially for screening tests, two single-blind control inhalation tests preceded 30 min by placebo or salmeterol and three allergen inhalation tests preceded by placebo, salmeterol or beclomethasone double-blind in random order. Airway responsiveness to methacholine (assessed as the provocative concentration of methacholine producing 20% fall in forced expiratory volume in one second (PC20)), induced sputum eosinophils, blood eosinophils and serum eosinophil cationic protein (ECP) were examined before and 7-48 h after treatment. The statistical power to detect twofold changes in blood and sputum parameters was &gt; or = 90%. Salmeterol inhaled before allergen challenge completely prevented the early asthmatic response, late asthmatic response and fall in methacholine PC20 at 24 h, and produced additional bronchodilatation. These effects were similar to those obtained by the inhalation of a single dose of salmeterol before the control inhalation test, and significantly better than those observed after a single dose of beclomethasone inhaled before the allergen test. Beclomethasone had no effect on the early asthmatic response or on the fall in methacholine PC20 at 24 h but partially inhibited the late asthmatic response. Neither salmeterol nor beclomethasone had any significant effect on sputum or blood inflammatory changes 7-48 h after allergen inhalation. In conclusion, whilst salmeterol had no demonstrable anti-inflammatory action in sputum after allergen challenge in asthma, neither did a single dose of the positive anti-inflammatory control, beclomethasone. The latter result excludes a more positive judgement on the possible anti-inflammatory action of salmeterol. However, the results do indicate that potent functional effects of a single dose of salmeterol can mask the airway inflammatory cell influx caused by inhaled allergen.
The exposome: a new paradigm to study the impact of environment on health
Authors: Martine Vrijheid
Journal: Thorax (2014)

Environmental factors, here taken to include pollutants, lifestyle factors and behaviours, can play an important role in serious, chronic pathologies with large societal and economic costs, including respiratory disease. However, measurement of the environmental component in epidemiological studies has traditionally relied on much more uncertain and incomplete assessments than measurement of the genome. The 'exposome' has therefore been proposed as a new paradigm to encompass the totality of human environmental (meaning all non-genetic) exposures from conception onwards, complementing the genome. Evidently, there are large challenges in developing the exposome concept into a workable approach for epidemiological research. These include: (1) the accurate and reliable measurement of many exposures in the external environment, (2) the measurement of a wide range of biological responses in the internal environment, and (3) addressing the dynamic, life course nature of the exposome. New tools and technologies that can be applied to address these challenges include exposure biomarker technologies, geographical mapping and remote sensing technologies, smartphone applications and personal exposure sensors, and high-throughput molecular 'omics' techniques. Prospective, population-based cohort studies have recently started to implement these methods using the exposome framework. The exposome thus offers a new and exciting paradigm for improvement and integration of currently scattered and uncertain data on the environmental component in disease aetiology. This should lead to a better understanding of the role of environmental risk factors in respiratory disease and other chronic pathologies, and ultimately to better primary prevention strategies.
Tripeptidyl Peptidase II Plays a Role in the Radiation Response of Selected Primary Cell Types but not Based on Nuclear Translocation and p53 Stabilization
Authors: Elke Firat, Chizuko Tsurumi, Simone Gaedicke, Jisen Huai, Gabriele Niedermann
Journal: Cancer Research (2009)

The giant cytosolic protease tripeptidyl peptidase II (TPPII) was recently proposed to play a role in the DNA damage response. Shown were nuclear translocation of TPPII after gamma-irradiation, lack of radiation-induced p53 stabilization in TPPII-siRNA-treated cells, and complete tumor regression in mice after gamma-irradiation when combined with TPPII-siRNA silencing or a protease inhibitor reported to inhibit TPPII. This suggested that TPPII could be a novel target for tumor radiosensitization and prompted us to study radiation responses using TPPII-knockout mice. Neither the sensitivity to total body irradiation nor the radiosensitivity of resting lymphoid cells, which both strongly depend on p53, was altered in the absence of TPPII. Functional integrity of p53 in TPPII-knockout cells is further shown by a proper G(1) arrest and by the accumulation of p53 and its transcriptional targets, p21, Bax, and Fas, on gamma-irradiation. Furthermore, we could not confirm radiation-induced nuclear translocation of TPPII. Nevertheless, after gamma-irradiation, we found slightly increased mitotic catastrophe of TPPII-deficient primary fibroblasts and increased apoptosis of TPPII-deficient activated CD8(+) T cells. The latter was accompanied by delayed resolution of the DNA double-strand break marker gammaH2AX. This could, however, be due to increased apoptotic DNA damage rather than reduced DNA damage repair. Our data do not confirm a role for TPPII in the DNA damage response based on nuclear TPPII translocation and p53 stabilization but nevertheless do show increased radiation-induced cell death of selected nontransformed cell types in the absence of the TPPII protease.
Transforming Growth Factor-β Signaling Promotes Pulmonary Hypertension Caused by <i>Schistosoma Mansoni</i>
Authors: Brian B. Graham, Jacob Chabon, Liya Gebreab, Jennifer Poole, Elias Debella, Laura Davis, Takeshi Tanaka, Linda Sanders, Nina Dropcho, Angela Bandeira, R. William Vandivier, Hunter C. Champion, Ghazwan Butrous, Xiao-Jing Wang, Thomas A. Wynn, Rubin M. Tuder
Journal: Circulation (2013)

The pathogenic mechanisms underlying pulmonary arterial hypertension resulting from schistosomiasis, one of the most common causes of pulmonary hypertension worldwide, remain unknown. We hypothesized that transforming growth factor-β (TGF-β) signaling as a consequence of Th2 inflammation is critical for the pathogenesis of this disease.Mice sensitized and subsequently challenged with Schistosoma mansoni eggs developed pulmonary hypertension associated with an increase in right ventricular systolic pressure, thickening of the pulmonary artery media, and right ventricular hypertrophy. Rho-kinase-dependent vasoconstriction accounted for ≈60% of the increase in right ventricular systolic pressure. The pulmonary vascular remodeling and pulmonary hypertension were dependent on increased TGF-β signaling, as pharmacological blockade of the TGF-β ligand and receptor, and mice lacking Smad3 were significantly protected from Schistosoma-induced pulmonary hypertension. Blockade of TGF-β signaling also led to a decrease in interleukin-4 and interleukin-13 concentrations, which drive the Th2 responses characteristic of schistosomiasis lung pathology. Lungs of patients with schistosomiasis-associated pulmonary arterial hypertension have evidence of TGF-β signaling in their remodeled pulmonary arteries.Experimental S mansoni-induced pulmonary vascular disease relies on canonical TGF-β signaling.