tbuckley/cabot-search huggingface dataset:
Collagenase production by rheumatoid synovial cells: morphological and immunohistochemical studies of the dendritic cell.
Authors: D E Woolley, C E Brinckerhoff, C L Mainardi, C A Vater, J M Evanson, E D Harris
Journal: Annals of the Rheumatic Diseases (1979)

The dendritic cells of dissociated, adherent rheumatoid synovial cell cultures are recognised by their distinctive morphological features-compact cytoplasm around the nucleus and long, branched cytoplasmic extensions.Such cells usually composed approximately 10% of the total adherent cell population but could vary from as few as 2 % to as many as 40 % with different synovial specimens.Histological studies have shown the cells to contain many mitochondria and large, spherical cytoplasmic inclusions which often distort the dendritic extensions.Although lysosomes were observed, no evidence for phagocytic activity was obtained.Immunolocalisation studies by means of a monospecific antibody to human collagenase have shown that the dendritic cell attached to a collagenous substratum produces and releases this enzyme in vitro.In contrast collagenase was detected in only a few ofthe fibroblastand macrophage-like cells, and it was always intracellular.It is proposed that the dendritic cell may have an important role in the pathophysiology of the rheu- matoid joint, particularly with regard to collagenase-mediated cartilage destruction.The ability of rheumatoid synovial collagenase to degrade cartilage collagen and insoluble tissue collagens (Harris and McCroskery, 1974; Woolley et al., 1975a, 1975b), and the recent immuno- localisation of this enzyme at the cartilage-pannus junction of rheumatoid joints (Woolley et al., 1977) support the view that collagenase plays an important role in the pathophysiology of the rheumatoid joint.The collagenase used in most studies to date has been obtained from the serum-free culture medium (Evanson et al., 1968) of rheumatoid synovial tissue explants.However, Dayer et al. (1976) recently reported that monolayer cultures of dissociated, adherent rheumatoid synovial cells released relatively large quantities of enzyme and prostaglandins.Such cultures also revealed an unusual cell type, described as 'stellate' (Dayer et al.
Inhibition of Interferon Gamma Production by Benzene and Benzene Metabolites
Authors: S. C. Cheung, D. E. Nerland, G. Sonnenfeld
Journal: JNCI Journal of the National Cancer Institute (1988)

We exposed Spleen cells from female Swiss/Webster mice to benzene and benaene metabolites to determine the effects of such exposure on interferon gamma induction by concanavalin A Exposting the cells to henzene or phenol did not affet interferon gamma production, but exposing them to p-benz oquinone, catechol, or hydroquinone significantiy inhibited interferon gamma production. cell viability, as determined by trypan blue viability standing, was not influenced by the chemical treatment, When interferon gamma production was inhibited, the inhibition was does dependent. The time of optimum Production of interferron gamma afer exposure to concanavalin A was not affected by treatment of the cells with p-benzoquinone. These data indicate the importance of dihydroxy and diketo metabolites as immunotoxic derivatives of benzene. [J Natl Cancer Inst 1988;80:1069–1072]
Transglutaminase 2 as an independent prognostic marker for survival of patients with non-adenocarcinoma subtype of non-small cell lung cancer
Authors: Chang-Min Choi, Se-Jin Jang, Seong-Yeol Park, Yong-Bock Choi, Jae-Heon Jeong, Dae-Seok Kim, Hyun-Kyoung Kim, Kang-Seo Park, Byung-Ho Nam, Hyeong-Ryul Kim, Soo-Youl Kim, Kyeong-Man Hong
Journal: Molecular Cancer (2011)

Abstract Background Expression of transglutaminase 2 (TGase 2) is related to invasion and resistance to chemotherapeutic agents in several cancer cells. However, there has been only limited clinical validation of TGase 2 as an independent prognostic marker in cancer. Methods The significance of TGase 2 expression as an invasive/migratory factor was addressed by in vitro assays employing down-regulation of TGase 2. TGase 2 expression as a prognostic indicator was assessed in 429 Korean patients with early-stage non-small cell lung cancer (NSCLC) by immunohistochemical staining. Results TGase 2 expression increased the invasive and migratory properties of NSCLC cells in vitro , which might be related to the induction of MMP-9. In the analysis of the immunohistochemical staining, TGase 2 expression in tumors was significantly correlated with recurrence in NSCLC (p = 0.005) or in the non-adenocarcinoma subtype (p = 0.031). Additionally, a multivariate analysis also showed a significant correlation between strong TGase 2 expression and shorter disease-free survival (DFS) in NSCLC (p = 0.029 and HR = 1.554) and in the non-adenocarcinoma subtype (p = 0.030 and HR = 2.184). However, the correlation in the adenocarcinoma subtype was not significant. Conclusions TGase 2 expression was significantly correlated with recurrence and shorter DFS in NSCLC, especially in the non-adenocarcinoma subtype including squamous cell carcinoma.
Epithelial-Mesenchymal Transition Induced by Growth Suppressor p12CDK2-AP1 Promotes Tumor Cell Local Invasion but Suppresses Distant Colony Growth
Authors: Takanori Tsuji, Soichiro Ibaragi, Kaori Shima, Miaofen G. Hu, Miki Katsurano, Akira Sasaki, Guo-fu Hu
Journal: Cancer Research (2008)

Abstract Epithelial-mesenchymal transition (EMT) has been considered essential for metastasis, a multistep process including local invasion, intravasation, extravasation, and proliferation at distant sites. However, controversy remains as to whether EMT truly happens and how important it is to metastasis. We studied the involvement of EMT in individual steps of metastasis and found that p12CDK2-AP1, a down-stream effector of transforming growth factor β, induced EMT of hamster cheek pouch carcinoma-1 cells by promoting the expression of Twist2. EMT cells have an increased invasive but decreased metastatic phenotype. When s.c. inoculated, both EMT and non-EMT cells established primary tumors, but only EMT cells invaded into the adjacent tissues and blood vessels; however, neither cells formed lung metastases. When i.v. inoculated, only non-EMT cells established lung metastases. Moreover, s.c. inoculation of a mixture of the two cell types resulted in intravasation of both cell types and formation of lung metastasis from non-EMT cells. Our results allowed us to propose a novel model for the role of EMT in cancer metastasis. We showed that EMT and non-EMT cells cooperate to complete the spontaneous metastasis process. We thus hypothesize that EMT cells are responsible for degrading the surrounding matrix to lead the way of invasion and intravasation. Non-EMT cells then enter the blood stream and reestablish colonies in the secondary sites. [Cancer Res 2008;68(24):10377–86]
RAGE signaling sustains inflammation and promotes tumor development
Authors: Christoffer Gebhardt, Astrid Riehl, Moritz Durchdewald, Julia Németh, Gerhard Fürstenberger, Karin Müller-Decker, Alexander Enk, Bernd Arnold, Angelika Bierhaus, Peter P. Nawroth, Jochen Hess, Peter Angel
Journal: The Journal of Experimental Medicine (2008)

A broad range of experimental and clinical evidence has highlighted the central role of chronic inflammation in promoting tumor development. However, the molecular mechanisms converting a transient inflammatory tissue reaction into a tumor-promoting microenvironment remain largely elusive. We show that mice deficient for the receptor for advanced glycation end-products (RAGE) are resistant to DMBA/TPA-induced skin carcinogenesis and exhibit a severe defect in sustaining inflammation during the promotion phase. Accordingly, RAGE is required for TPA-induced up-regulation of proinflammatory mediators, maintenance of immune cell infiltration, and epidermal hyperplasia. RAGE-dependent up-regulation of its potential ligands S100a8 and S100a9 supports the existence of an S100/RAGE-driven feed-forward loop in chronic inflammation and tumor promotion. Finally, bone marrow chimera experiments revealed that RAGE expression on immune cells, but not keratinocytes or endothelial cells, is essential for TPA-induced dermal infiltration and epidermal hyperplasia. We show that RAGE signaling drives the strength and maintenance of an inflammatory reaction during tumor promotion and provide direct genetic evidence for a novel role for RAGE in linking chronic inflammation and cancer.
Serotonin Induces Mast Cell Adhesion and Chemotaxis through the 5-HT1A Receptor
Authors: N.M. Kushnir-Sukhov, A.M. Gilfillan, J.W. Coleman, M. Toth, S. Bruening, D.D. Metcalfe
Journal: Journal of Allergy and Clinical Immunology (2006)
Electrohydraulic lithotripsy of large bile duct stones under direct cholangioscopy with a double-balloon endoscope
Authors: Ryunosuke Hakuta, Hirofumi Kogure, Hiroyuki Isayama, Atsuo Yamada, Tsuyoshi Hamada, Yousuke Nakai, Kazuhiko Koike
Journal: Endoscopy (2015)

The use of a short double-balloon endoscope facilitates the endoscopic removal of bile duct stones in patients with surgically altered anatomy [1] [2]. However, the narrow and long working channel of the double-balloon endoscope occasionally makes the procedure difficult and time-consuming. Herein, we present the case of a patient with a history of hepaticojejunostomy in whom large bile duct stones were successfully fragmented and removed under direct visualization with a short double-balloon endoscope and electrohydraulic lithotripsy (EHL).
Respiratory Syncytial Virus Infection in Immunocompromised Adults
Authors: Janet A. Englund
Journal: Annals of Internal Medicine (1988)

Respiratory syncytial virus disease was documented in 11 immunocompromised adults, aged 21 to 50. Underlying conditions included bone marrow transplant (6 patients), renal transplant (3 patients), renal and pancreas transplants (1 patient), and T-cell lymphoma (1 patient). Diagnosis of infection was based on specimens from bronchoalveolar lavage, sputum, throat, sinus aspirate, and lung biopsy. The virus was detected simultaneously by antibody in either an immunofluorescence or enzyme-linked immunosorbent assay in 3 of 4 patients whose culture results were positive for respiratory syncytial virus. The virus was an unexpected finding, despite widespread infection in the community. Clinical symptoms included low-grade fever, nonproductive cough, rhinorrhea or nasal congestion, and radiographic evidence of interstitial infiltrates and sinusitis. Aerosolized ribavirin therapy was used in the 6 recipients of bone marrow transplants, 3 of whom required assisted ventilation but died. Death caused by virus infection was documented in 4 of 11 patients. Respiratory syncytial virus disease must be considered in the differential diagnosis of fever and pulmonary infiltrates in immunocompromised adults.
Evolving Trends and Treatment Advances in Pediatric Poisoning
Authors: E L Liebelt, C D DeAngelis
Journal: JAMA (1999)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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
<i>CMTM3</i>, Located at the Critical Tumor Suppressor Locus 16q22.1, Is Silenced by CpG Methylation in Carcinomas and Inhibits Tumor Cell Growth through Inducing Apoptosis
Authors: Yu Wang, Jisheng Li, Yan Cui, Ting Li, Ka Man Ng, Hua Geng, Henan Li, Xing-sheng Shu, Hongyu Li, Wei Liu, Bing Luo, Qian Zhang, Tony Shu Kam Mok, Wei Zheng, Xiaoyan Qiu, Gopesh Srivastava, Jun Yu, Joseph J.Y. Sung, Anthony T.C. Chan, Dalong Ma, Qian Tao, Wenling Han
Journal: Cancer Research (2009)

Closely located at the tumor suppressor locus 16q22.1, CKLF-like MARVEL transmembrane domain-containing member 3 and 4 (CMTM3 and CMTM4) encode two CMTM family proteins, which link chemokines and the transmembrane-4 superfamily. In contrast to the broad expression of both CMTM3 and CMTM4 in normal human adult tissues, only CMTM3 is silenced or down-regulated in common carcinoma (gastric, breast, nasopharyngeal, esophageal, and colon) cell lines and primary tumors. CMTM3 methylation was not detected in normal epithelial cell lines and tissues, with weak methylation present in only 5 of 35 (14%) gastric cancer adjacent normal tissues. Furthermore, immunohistochemistry showed that CMTM3 protein was absent in 12 of 35 (34%) gastric and 1 of 2 colorectal tumors, which was well correlated with its methylation status. The silencing of CMTM3 is due to aberrant promoter CpG methylation that could be reversed by pharmacologic demethylation. Ectopic expression of CMTM3 strongly suppressed the colony formation of carcinoma cell lines. In addition, CMTM3 inhibited tumor cell growth and induced apoptosis with caspase-3 activation. Thus, CMTM3 exerts tumor-suppressive functions in tumor cells, with frequent epigenetic inactivation by promoter CpG methylation in common carcinomas.
C. elegans ORFeome version 1.1: experimental verification of the genome annotation and resource for proteome-scale protein expression
Authors: Jérôme Reboul, Philippe Vaglio, Jean-François Rual, Philippe Lamesch, Monica Martinez, Christopher M. Armstrong, Siming Li, Laurent Jacotot, Nicolas Bertin, Rekin's Janky, Troy Moore, James R. Hudson, James L. Hartley, Michael A. Brasch, Jean Vandenhaute, Simon Boulton, Gregory A. Endress, Sarah Jenna, Eric Chevet, Vasilis Papasotiropoulos, Peter P. Tolias, Jason Ptacek, Mike Snyder, Raymond Huang, Mark R. Chance, Hongmei Lee, Lynn Doucette-Stamm, David E. Hill, Marc Vidal
Journal: Nature Genetics (2003)
Area-level socio-economic status and health status among adults with asthma and rhinitis
Authors: P. D. Blanc
Journal: European Respiratory Journal (2005)

Socio-economic status (SES) may affect health status in airway disease at the individual and area level. In a cohort of adults with asthma, rhinitis or both conditions, questionnaire-derived individual-level SES and principal components analysis (PCA) of census data for area-level SES factors were used. Regression analysis was utilised to study the associations among individual- and area-level SES for the following four health status measures: severity of asthma scores and the Short Form-12 Physical Component Scale (SF-12 PCS) (n = 404); asthma-specific quality of life (QoL) scores (n = 340); and forced expiratory volume in one second (FEV<sub>1</sub>) per cent predicted (n = 218). PCA yielded a two-factor solution for area-level SES. Factor 1 (lower area-level SES) was significantly associated with poorer SF-12 PCS and worse asthma QoL. These associations remained significant after adding individual-level SES. Factor 1 was also significantly associated with severity of asthma scores, but not after addition of the individual-level SES. Factor 2 (suburban area-level SES) was associated with lower FEV<sub>1</sub> per cent predicted in combined area-level and individual SES models. In conclusion, area-level socio-economic status is linked to some, but not all, of the studied health status measures after taking into account individual-level socio-economic status.
Conserved Primers for Rapid Sequencing of the Complete Mitochondrial Genome from Carnivores, Applied to Three Species of Bears
Authors: Isabelle Delisle, Curtis Strobeck
Journal: Molecular Biology and Evolution (2002)

Phylogenetic relationships of the order Carnivora have been extensively studied. However, depending on the type of data, species sampling, and method of analysis used, carnivores have been placed in nearly every possible position throughout the eutherian phylogenetic tree (for a review, see Novacek 1992). The integrity of the order itself has, however, remained intact. Undisputedly monophyletic, the order Carnivora nonetheless constitutes a very adaptable and heterogeneous group (Wayne et al. 1989) whose evolution has been marked by several events of parallel or convergent evolution and rapid radiation. Consequently, phylogenetic relationships between and within many carnivore families are also still largely unresolved. For example, the families Procyonidae, Ailuridae, Mustelidae, Pinnidedia, and Ursidae are joined at a polytomy. Within Pinnipedia, the closer affinity of Otariidae to either Phocidae or Obodenidae has long been debated. Additionally, the monophyly of the family Mustelidae has been challenged, with true mustelids and mephitids thought to belong to different branches within the superfamily Musteloidea, also including Procyonidae and Ailuridae. The phylogeny of the family Ursidae is another typical example. Six species of bears, grouped under the subfamily Ursinae, are thought to have diverged at the beginning of the Pliocene through such a rapid radiation event (Thenius 1990) that the order of species divergence is difficult to determine. Hence, the speciation event that led to extant ursine bears (American black bear, Ursus americanus; brown bear, U. arctos; polar bear, U. maritimus; Asiatic black bear, U. thibetanus; sun bear, U. malayanus; and sloth bear, U. ursinus) is usually represented as a polytomy. Rapid radiations remain unresolved largely because available data contain very few informative changes essential to infer the correct phylogenetic tree. More resolving power can be reached by using longer DNA sequences to provide a sufficient number of informative characters. Moreover, it has been shown that the combination of multiple genes in a single large data set has the potential to raise a weak phylogenetic signal above the noise level (Bull et al. 1993). Combining these two advantages, complete mitochondrial (mtDNA) sequences (approximately 17 kbp and 13 protein-coding genes) offer great potential for recovering phylogenies.
Sensitivity of reticulocyte indices to iron therapy in an intensely training athlete
Authors: M J Ashenden, G P Dobson, A G Hahn
Journal: British Journal of Sports Medicine (1998)

Iron deficiency anaemia, and its debilitating effect on performance, is an area of concern for many female athletes. Automated technologies that analyse individual reticulocytes may provide a sensitive measure of bone marrow response to iron supplementation. The reticulocyte characteristics of a female volleyball player with frank iron deficiency anaemia, and her subsequent response to oral iron therapy, are reported.
Comparison of Different Adult Stem Cell Types for Treatment of Myocardial Ischemia
Authors: Koen E.A. van der Bogt, Ahmad Y. Sheikh, Sonja Schrepfer, Grant Hoyt, Feng Cao, Katherine J. Ransohoff, Rutger-Jan Swijnenburg, Jeremy Pearl, Andrew Lee, Michael Fischbein, Christopher H. Contag, Robert C. Robbins, Joseph C. Wu
Journal: Circulation (2008)

A comparative analysis of the efficacy of different cell candidates for the treatment of heart disease remains to be described. This study is designed to evaluate the therapeutic efficacy of 4 cell types in a murine model of myocardial infarction.Bone marrow mononuclear cells (MN), mesenchymal stem cells (MSC), skeletal myoblasts (SkMb), and fibroblasts (Fibro) expressing firefly luciferase (Fluc) and green fluorescence protein (GFP) were characterized by flow cytometry, bioluminescence imaging (BLI), and luminometry. Female FVB mice (n=70) underwent LAD ligation and intramyocardially received one cell type (5x10(5)) or PBS. Cell survival was measured by BLI and by TaqMan PCR. Cardiac function was assessed by echocardiography and invasive hemodynamic measurements. Fluc expression correlated with cell number in all groups (r(2)>0.93). In vivo BLI revealed acute donor cell death of MSC, SkMb, and Fibro within 3 weeks after transplantation. By contrast, cardiac signals were still present after 6 weeks in the MN group, as confirmed by TaqMan PCR (P<0.01). Echocardiography showed significant preservation of fractional shortening in the MN group compared to controls (P<0.05). Measurements of left ventricular end-systolic/diastolic volumes revealed that the least amount of ventricular dilatation occurred in the MN group (P<0.05). Histology confirmed the presence of MN, although there was no evidence of transdifferentiation by donor MN into cardiomyocytes.This is the first study to show that compared to MSC, SkMB, and Fibro, MN exhibit a more favorable survival pattern, which translates into a more robust preservation of cardiac function.
The kinase mTOR regulates the differentiation of helper T cells through the selective activation of signaling by mTORC1 and mTORC2
Authors: Greg M Delgoffe, Kristen N Pollizzi, Adam T Waickman, Emily Heikamp, David J Meyers, Maureen R Horton, Bo Xiao, Paul F Worley, Jonathan D Powell
Journal: Nature Immunology (2011)
Lipoprotein lipase-mediated uptake and degradation of low density lipoproteins by fibroblasts and macrophages.
Authors: S C Rumsey, J C Obunike, Y Arad, R J Deckelbaum, I J Goldberg
Journal: Journal of Clinical Investigation (1992)

Lipoprotein lipase (LPL), the rate limiting enzyme for hydrolysis of lipoprotein triglyceride, also mediates nonenzymatic interactions between lipoproteins and heparan sulfate proteoglycans. To determine whether cell surface LPL increases LDL binding to cells, bovine milk LPL was added to upregulated and nonupregulated human fibroblasts along with media containing LDL. LDL binding to cells was increased 2-10-fold, in a dose-dependent manner, by the addition of 0.5-10 micrograms/ml of LPL. The amount of LDL bound to the cells in the presence of LPL far exceeded the capacity for LDL binding via the LDL receptor. Treatment of fibroblasts with heparinase and heparitinase resulted in a 64% decrease in LPL-mediated LDL binding. Compared to studies performed without LPL, more LDL was internalized and degraded in the presence of LPL, but the time course was slower than that of classical lipoprotein receptor mediated pathways. In LDL receptor negative fibroblasts, LPL increased surface bound LDL > 140-fold, intracellular LDL > 40-fold, and LDL degradation > 6-fold. These effects were almost completely inhibited by heparin and anti-LPL monoclonal antibody. LPL also increased the binding and uptake by fibroblasts of apolipoprotein-free triglyceride emulsions; binding was increased > 8-fold and cellular uptake was increased > 40-fold with LPL. LPL increased LDL binding to THP-1 monocytes, and increased LDL uptake (4.5-fold) and LDL degradation (2.5-fold) by THP-1 macrophages. In the absence of added LPL, heparin and anti-LPL monoclonal antibodies decreased LDL degradation by > 40%, and triglyceride emulsion uptake by > 50%, suggesting that endogenously produced LPL mediated lipid particle uptake and degradation. We conclude that LPL increases lipid and lipoprotein uptake by cells via a pathway not involving the LDL receptor. This pathway may be important for lipid accumulation in LPL synthesizing cells.