tbuckley/cabot-search huggingface dataset:
The impact of pollution on allergic disease
Authors: C. Rusznak, J. L. Devalia, R. J. Davies
Journal: Allergy (1994)

Evidence suggests that allergic disease is becoming more common, particularly in industrialized societies. Two studies of schoolchildren from Aberdeen, Scotland aged 8–13 years were undertaken in 1964 and 1989 using identical questionnaires, and found that the reported prevalence of asthma had risen from 4.1% to 10.2% during this period, hay fever from 3.2% to 11.9% and eczema from 5.3% to 12%. Indication that air pollution may contribute to this increase has come from several studies. In Japan, allergic rhinoconjunctivitis was found to be more prevalent in individuals living near motorways than in cedar forests. Severe asthma also occurs more commonly than mild asthma in children living in polluted areas. Exercise‐induced asthma and the use of asthma medication were twice as high in a town near two power stations compared with a non‐polluted town. A recent study in Finland showed that admissions to hospital with severe asthma correlated with atmospheric levels of nitrogen dioxide. Deterioration in peak flow recordings in asthmatics and exacerbations of symptoms in hay fever sufferers correlate with ambient levels of ozone. Elucidation of the mechanisms by which exposure to air pollutants may influence the frequency of allergic disease or exacerbate symptoms has come from in vitro and in vivo experiments in animals and man. Animals exposed to ozone, sulphur dioxide, nitrogen dioxide and particles from diesel exhaust, together with allergens, show more ready development of allergic sensitization compared with those exposed to allergen alone. The dose of allergen necessary to produce a 20% fall in FEV 1 (forced expiratory volume in 1 second) in mild asthmatics is reduced by previous exposure to ozone or a mixture of nitrogen dioxide and sulphur dioxide. It has also been suggested that the allergic potency of pollen grains may be increased when they are coated in pollutants. Bronchial and nasal lavage studies have shown that air pollutants can induce an influx of inflammatory cells and proinflammatory cytokines into the respiratory tract. Studies on human epithelial cells cultured to confluence in vitro have indicated that exposure to nitrogen dioxide can decrease ciliary beat frequency which would, in theory, reduce allergen clearance and increase the risk of sensitization. Further, exposure of these cells to either ozone or nitrogen dioxide induces the release of inflammatory mediators, such as leukotriene C 4 , and proinflammatory cytokines, including granulocyte‐macrophage colony‐stimulating factor, tumour necrosis factor‐α and interleukin‐8. This effect can be attenuated by the use of anti‐inflammatory drugs.
922 Immunohistochemical study of cytokin producing cells in Peyer's patch and intestinal lamina propria of ovalbumin (OVA)— Sensitized BALB/c mouse
Authors: M VINUESA, Y TANAKA, T MATSUSHITA, J KAKUGAWA, H YOSHIDA, J GALIMANY
Journal: Journal of Allergy and Clinical Immunology (1996)
The novel JAK inhibitor AZD1480 blocks STAT3 and FGFR3 signaling, resulting in suppression of human myeloma cell growth and survival
Authors: A Scuto, P Krejci, L Popplewell, J Wu, Y Wang, M Kujawski, C Kowolik, H Xin, L Chen, Y Wang, L Kretzner, H Yu, W R Wilcox, Y Yen, S Forman, R Jove
Journal: Leukemia (2010)
Role of common and rare variants in <i>SCN10A</i>: results from the Brugada syndrome QRS locus gene discovery collaborative study
Authors: Elijah R. Behr, Eleonora Savio-Galimberti, Julien Barc, Anders G. Holst, Evmorfia Petropoulou, Bram P. Prins, Javad Jabbari, Margherita Torchio, Myriam Berthet, Yuka Mizusawa, Tao Yang, Eline A. Nannenberg, Federica Dagradi, Peter Weeke, Rachel Bastiaenan, Michael J. Ackerman, Stig Haunso, Antoine Leenhardt, Stefan Kääb, Vincent Probst, Richard Redon, Sanjay Sharma, Arthur Wilde, Jacob Tfelt-Hansen, Peter Schwartz, Dan M. Roden, Connie R. Bezzina, Morten Olesen, Dawood Darbar, Pascale Guicheney, Lia Crotti, Yalda Jamshidi
Journal: Cardiovascular Research (2015)

Brugada syndrome (BrS) remains genetically heterogeneous and is associated with slowed cardiac conduction. We aimed to identify genetic variation in BrS cases at loci associated with QRS duration. A multi-centre study sequenced seven candidate genes (SCN10A, HAND1, PLN, CASQ2, TKT, TBX3, and TBX5) in 156 Caucasian SCN5A mutation-negative BrS patients (80% male; mean age 48) with symptoms (64%) and/or a family history of sudden death (47%) or BrS (18%). Forty-nine variants were identified: 18 were rare (MAF <1%) and non-synonymous; and 11/18 (61.1%), mostly in SCN10A, were predicted as pathogenic using multiple bioinformatics tools. Allele frequencies were compared with the Exome Sequencing and UK10K Projects. SKAT methods tested rare variation in SCN10A finding no statistically significant difference between cases and controls. Co-segregation analysis was possible for four of seven probands carrying a novel pathogenic variant. Only one pedigree (I671V/G1299A in SCN10A) showed co-segregation. The SCN10A SNP V1073 was, however, associated strongly with BrS [66.9 vs. 40.1% (UK10K) OR (95% CI) = 3.02 (2.35–3.87), P = 8.07 × 10–19]. Voltage-clamp experiments for NaV1.8 were performed for SCN10A common variants V1073, A1073, and rare variants of interest: A200V and I671V. V1073, A200V and I671V, demonstrated significant reductions in peak INa compared with ancestral allele A1073 (rs6795970). Rare variants in the screened QRS-associated genes (including SCN10A) are not responsible for a significant proportion of SCN5A mutation negative BrS. The common SNP SCN10A V1073 was strongly associated with BrS and demonstrated loss of NaV1.8 function, as did rare variants in isolated patients.
627 HBV SUPPRESSES TLR SIGNALING AND THE CROSSTALK TO THE ADAPTIVE IMMUNE SYSTEM IN MURINE AND HUMAN CELLS
Authors: M. Jiang, M. Trippler, R. Broering, L. Poggenpohl, J. Wu, M. Roggendorf, G. Gerken, M. Lu, J. Schlaak
Journal: Journal of Hepatology (2010)
Glucocorticoids induce differentiation of a specifically activated, anti-inflammatory subtype of human monocytes
Authors: Jan Ehrchen, Lars Steinmüller, Katarzyna Barczyk, Klaus Tenbrock, Wolfgang Nacken, Martin Eisenacher, Ursula Nordhues, Clemens Sorg, Cord Sunderkötter, Johannes Roth
Journal: Blood (2006)
Understanding Cancer: From Basic Science to Clinical Practice
Authors: Dante G. Scarpelli
Journal: Annals of Internal Medicine (1997)

Medical Writings15 November 1997Understanding Cancer: From Basic Science to Clinical PracticeDante G. Scarpelli, MD, PhDDante G. Scarpelli, MD, PhDNorthwestern University Medical School, Chicago, IllinoisSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-127-10-199711150-00020 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Alison MR, Sarraf CE. 269 pages. New York: Cambridge Univ Pr; 1997. $29.95. ISBN 0521567513. Order phone 800-872-7423.Field of medicine: Oncology and cancer biology.Format: Softcover book.Audience: Medical and graduate students, scientists involved in cancer research, and physicians seeking a clear understanding of cancer biology and contemporary cancer therapy.Purpose: To introduce the principles of cancer biology and clinical oncology.Content: This primer presents the major biological and clinical features of cancer in an organized, brief, and focused manner. In its short span of 269 pages, it offers a surprisingly well-integrated and cogent survey of the field. An ... Author, Article, and Disclosure InformationAffiliations: Northwestern University Medical School, Chicago, Illinois PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 November 1997Volume 127, Issue 10Page: 949KeywordsCancer geneticsCancer treatmentCell proliferationGenetic causes of cancerGraduate medical educationGrowth factorsMolecular biologyPolymerase chain reactionScientistsStem cells ePublished: 15 August 2000 Issue Published: 15 November 1997 Copyright & PermissionsCopyright © 1997 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Primary Adenocarcinoma of the Appendix
Authors: Alexander Gerber, Abraham Mackles, Adolph P. Raab
Journal: New England Journal of Medicine (1954)

PRIMARY adenocarcinoma of the appendix is a rare disease. Young and Wyman1 carefully searched the literature from 1932 to 1942 and found only 4 bona-fide cases2 3 4 5; they added a fifth. In 1943 Uihlein and McDonald6 contributed greatly to the understanding of this disease by classification into three types: carcinoid; malignant mucocele; and adenocarcinoma of the colonic type. Over a thirty-year period at the Mayo Clinic 5 cases of the colonic type had occurred. Ehrlich and Hunter7 studied 813 gastrointestinal tumors in men of military age during World War II. Of these, 441 were malignant, including 7 primary in the . . .
Use of recombinant hirudin as antithrombotic treatment in patients with heparin‐induced thrombocytopenia
Authors: F. Schiele, A. Vuillemenot, P. Kramarz, Y. Kieffer, T. Anguenot, Y. Bernard, J. P. Bassand
Journal: American Journal of Hematology (1995)

Abstract Heparin‐induced thrombocytopenia is a rare but severe complication of heparin therapy that can result in severe venous or arterial thromboembolic events and whose treatment remains partially unanswered. Recombinant hirudin is potentially effective as an antithrombotic treatment in the management of heparin‐induced thrombocytopenia, given its potent antithrombin effects without known interaction with platelets. We report the results obtained with intravenous recombinant hirudin (HBW 023) administered on a compassionate basis to patients suffering from heparin‐induced thrombocytopenia. Six patients suffering from heparin‐induced thrombocytopenia were submitted to intravenous recombinant hirudin (HBW 023) administered at a dose of 0.05 mg/kg/hr after an initial bolus injection of 0.07 mg/kg in the case of a venous thromboembolic event, and at a dose of 0.15 mg/kg/hr with the same initial bolus injection in the case of an arterial thromboembolic event. Whenever possible, oral anticoagulation with acenocoumarol was introduced at the same time as recombinant hirudin, which was interrupted as soon as the international normalized ratio reached 3. Clinical events, particularly thromboembolism and bleeding, were noted; activated partial thromboplastin time (aPTT), and platelet count were assessed throughout the administration of recombinant hirudin. Heparins responsible for heparin‐induced thrombocytopenia were porcine sodium or calcium heparinate in four cases, nadroparin in one case, and enoxaparin in one case. Thrombocytopenia was discovered on routine systematic platelet count in two patients and after the occurrence of arterial and venous thromboembolism in two patients, respectively. After discontinuation of heparin and the onset of recombinant hirudin, clinical evolution was uneventful in all patients, with no recurrence of thromboembolism, limb amputation, or hemorrhagic complication. The aPTT ratio varied from 1.8 to 3.5 (median 2.4) throughout administration of recombinant hirudin. Platelet count rose from nadir (median value 60 × 10 9 15 to 90) to above 100 × 10 9 /L in every patient within 3–6 days (median 5), after discontinuation of heparin. Intravenous administration of recombinant hirudin ensured safe anticoagulation in patients with heparin‐induced thrombocytopenia and made it possible to wait for oral anticoagulation to become efficient and platelet count to return to normal values without occurrence or recurrence of thromboembolism.
TCT-906 Towards Simulation-Based Pre-Operative Planning Of Transcatheter Aortic Valve Replacement
Authors: Carl Schultz, Peter Mortier, Nico Bruining, Gianluca De Santis, Heleen van Beusekom, Patrick Segers, Robert-Jan van Geuns, Benedict Verhegghe, Nicolas Van Mieghem, Matthieu De Beule, Peter De Jaegere
Journal: Journal of the American College of Cardiology (2012)
Genome-Wide Association Studies, Alzheimer Disease, and Understudied Populations
Authors: Robert L. Nussbaum
Journal: JAMA (2013)

Genetics researchers have been grappling for decades with the problem of how to identify the genetic variants contributing to disease traits with complex inheritance. In common diseases such as type 2 diabetes, cardiovascular disease, and late-onset Alzheimer disease (LOAD), a contribution by genetic variants can be inferred because these diseases are �familial�; ie, the more genetically related a relative is to the affected person, the more frequently the relative is also affected.
Deaths and Cardiovascular Events in Men Receiving Testosterone
Authors: James Katz, Robert Nadelberg
Journal: JAMA (2014)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Antiretroviral therapy: new solutions bring new problems
Authors: J. L Atkins
Journal: BMJ (2003)

EDITOR—Jordan et al's meta-analysis of antiretroviral drug regimens supports the continued use of triple therapy for established HIV infections in adolescent and adult patients.1 While any advance in combating the progression of HIV is clearly welcome, the potential side effects of treatment need to be known.

Antiretroviral inhibitor use is associated with a range of morphological and metabolic alterations. Altered glucose homeostasis may result …
Survival role of protein kinase C (PKC) in chronic lymphocytic leukemia and determination of isoform expression pattern and genes altered by PKC inhibition
Authors: Serhan Alkan, Qin Huang, Melek Ergin, Mitchell F. Denning, Sucha Nand, Tazeen Maududi, Gladell P. Paner, Fulya Ozpuyan, Keith F. Izban
Journal: American Journal of Hematology (2005)

Recent studies have suggested that protein kinase C (PKC) activation plays an important role in survival of chronic lymphocytic leukemia (CLL). In order to characterize the role of PKC in CLL, we investigated the expression pattern of PKC isoforms in CLL cells (7 cases) and evaluated the effect of PKC inhibition on the survival of CLL cells (20 cases). Expression of the classical PKC isoforms beta and gamma, the novel isoform delta and the atypical isoform zeta was seen in all analyzed patient samples by Western blot analysis. Expression of the PKC isoforms alpha, epsilon, and iota was variable. Following incubation with the PKC inhibitor, safingol, CLL cells underwent marked apoptosis in all cases. In order to characterize the molecular events associated with the apoptotic effect of PKC inhibition, gene expression patterns in CLL cells were evaluated by cDNA-microarray analysis. Following safingol treatment, several genes showed marked downregulation and PKC-related proteins demonstrated decreased hybridization signals. Among these proteins, CREB and Daxx were further studied by using Western blotting, nuclear binding assay and confocal immunofluorescent microscopy. These studies showed significant inhibition of these proteins, consistent with the results of microarray gene analysis. Overall, these findings suggest that PKC activation is important for CLL cell survival and that inhibitors of PKC may have a role in the treatment of patients with CLL.
HLA class II peptide tetramers<i>vs</i>allergen-induced proliferation for identification of allergen-specific CD4 T cells
Authors: D. Van Hemelen, V. Mahler, G. Fischer, I. Fae, V. Reichl-Leb, W. Pickl, M. Jutel, S. Smolinska, C. Ebner, B. Bohle, B. Jahn-Schmid
Journal: Allergy (2014)

Fluorescence-labeled MHC class II/peptide tetramer complexes are considered as optimal tools to characterize allergen-specific CD4(+) T cells, but this technique is restricted to frequently expressed HLA class II molecules and knowledge of immunodominant epitopes. In contrast, allergen-stimulated proliferation assessed by CFSE dilution is less sophisticated and widely applicable. The major mugwort allergen, Art v 1, contains only one single, immunodominant, HLA-DR1-restricted epitope (Art v 125-36 ). Thus, essentially all Art v 1-reactive cells should be identified by a HLA-DRB1*01:01/Art v 119-36 tetramer.We compared specificity and sensitivity of tetramer(+) and allergen-induced proliferating (CFSE(lo) ) CD4(+) T cells by flow cytometry.The frequency of tetramer(+) CD4(+) T cells determined ex vivo in PBMC of mugwort-allergic individuals ranged from 0 to 0.029%. After 2-3 weeks of in vitro expansion, sufficient tetramer(+) T cells for phenotyping were detected in 83% of Art v 125-36 -reactive T-cell lines (TCL) from mugwort-allergic individuals, but not in TCL from healthy individuals. The tetramers defined bona fide Th2 cells. Notably, Art v 125-36 -reactive TCL depleted of tetramer(+) T cells still reacted to the peptide, and only 44% of Art v 125-36 -specific T-cell clones were detected by the tetramer. CFSE(lo) CD4(+) T cells contained only 0.3-10.7% of tetramer(+) T cells and very low proportions of Th2 cells.Allergen-specific T cells can be identified by HLA class II tetramers with high specificity, but unexpected low sensitivity. In contrast, allergen-stimulated CFSE(lo) CD4(+) T cells contain extremely high fractions of bystander cells. Therefore, for T-cell monitoring, either method should be interpreted with caution.
Abstract 2328: COX-2 induce mediated multidrug resistance by activating JNK signal transduction pathway in colorectal cancer
Authors: Qi Li, Hua Sui
Journal: Cancer Research (2014)

Abstract Chemotherapy is an important therapeutic option for most cancer patients; however, drug resistance causes the failure of chemotherapy and becomes a major obstacle for successful chemotherapy. The overexpression of P-gp has been associated with the resistance to a wide range of anticancer drugs. In the present study, drug-sensitive and multidrug resistant MDR colon carcinoma cell lines were used to examine the role of JNK signaling pathway in P-gp-mediated MDR associated with COX-2. We have found that sp600125, a JNK inhibitor or NS-398, a COX-2 inhibitor, reduced the degree of MDR in MDR cells. This phenomenon was accompanied by a significant decrease in gene level of ABCB1 and protein level of P-gp in MDR cells. In contrast, addition of a JNK inhibitor had no significant effect on the expression of COX-2. Interestingly, inhibition of COX-2 activity led to a decreased level of p-c-Jun at Ser63/73 due to JNK activation. In addition, there is an overexpression of p-c-Jun in MDR cells transfected with recombinant vector pGL3-Basic-COX-2 promoter. Moreover, the intracellular vincristine accumulation significantly increased with treatment of sp600125, or NS-398. In conclusion, our study has provided the first direct evidence that COX-2 induced up-regulation of P-gp in MDR cells, which was associated with an enhanced activity of the c-Jun phosphorylation at Ser63/73. Our findings may facilitate the development of novel antitumor drugs that are more effective against both chemosensitive and MDR cells. Note: This abstract was not presented at the meeting. Citation Format: Qi Li, Hua Sui. COX-2 induce mediated multidrug resistance by activating JNK signal transduction pathway in colorectal cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2328. doi:10.1158/1538-7445.AM2014-2328
Sudden large and periodic changes in heart rate in healthy young men after short periods of exercise.
Authors: S Jennett, J F Lamb, P Travis
Journal: BMJ (1982)

The instantaneous heart rate and respiratory pattern were recorded immediately after brief periods of exercise in 41 healthy male students. Recordings were taken with the subjects both supine and standing. More than half of these subjects showed oscillatory heart changes when recovering supine but not when standing. During these oscillations the heart rate slowed suddenly by more than 30 beats/min; the oscillations had a period of 4 to 8 seconds, and they continued for half to two minutes. The P waves of the electrocardiogram were decreased during the slowing, consistent with increased vagal activity. When these oscillations occurred they each followed the start of an inspiration with the same latency as in respiratory sinus arrhythmia; unlike respiratory sinus arrhythmia, however, they did not occur after every inspiration but varied from 1:1 to 1:3 oscillations:breaths. They were not usually stopped by breath holding but were reduced or abolished by procedures which reduced venous return. This pattern of oscillations--"vagushalt"--seems to be different from respiratory sinus arrhythmias, and central venous pressure may contribute to the phenomenon. Although it is not widely recognised, vagushalt is probably very common and possibly its occurrence may change in disease.
Dual Diagnosis in Substance Abuse
Authors: Alan L. Krueger
Journal: JAMA (1992)

Dual diagnosis has been a major focus in mental health care in recent years. Substance abuse occurring with any other psychopathology qualifies a patient for a dual diagnosis or multiple diagnosis. Treatment facilities have used this "new" concept to justify special treatment approaches and dual diagnosis units. Authors are writing about the biopsychosocial model of psychopathology as if it were a new discovery. The disease concept of addiction has been more clearly defined and accepted. All of these currents have helped therapists focus on treating multiple factors in human beings with illnesses and have generated a large literature on holistic therapy. Drs Gold and Slaby have gathered review articles on various aspects of dual diagnoses in patients with substance abuse, all of which concentrate on the biopsychosocial aspects of patient care. The text has three main sections. The introduction discusses the concept of dual diagnosis and the role of genetics
AN OPERATION FOR SPINA BIFIDA, WITH REPORT OF A SUCCESSFUL CASE.
Authors: LEONARD FREEMAN
Journal: JAMA (1902)

A spina bifida is a hernia of the membranes surrounding the spinal cord through a congenital opening in the posterior aspect of the spine. Very rarely there is also a defect in the bodies of the vertebræ. The sac is always filled with cerebrospinal fluid, and often contains nerves from the cauda equina, or a portion of the cord itself. The sac is usually covered by integument, but this is frequently so thin as to be translucent. The opening may be so small that it will scarcely admit the finest probe, or it may extend from the foramen magnum to the sacrum. Extensive deficiencies are, however, very rare. The tumor is usually located in the lumbo-sacral region, although it may appear at any point along the spine. It may be large or small, pedunculated or sessile. A meningocele is a hernia of the membranes containing fluid only; a meningo-myelocele contains