tbuckley/cabot-search huggingface dataset:
Cellulose‐Based Diagnostic Devices for Diagnosing Serotype‐2 Dengue Fever in Human Serum
Authors: Hsi‐Kai Wang, Cheng‐Han Tsai, Kuan‐Hung Chen, Chung‐Tao Tang, Jiun‐Shyang Leou, Pi‐Chun Li, Yin‐Liang Tang, Hsyue‐Jen Hsieh, Han‐Chung Wu, Chao‐Min Cheng
Journal: Advanced Healthcare Materials (2013)

Abstract Here, two types of cellulose‐based in vitro diagnostic devices are demonstrated for the diagnosis of dengue virus infection in both buffer system and human serum: 1) paper‐based ELISA for providing the semiquantitative information of the disease activity of serotype‐2 dengue fever to healthcare persons (i.e., monitoring the disease activity with a specific serotype in single patients); 2) lateral flow immunoassays to screen for infection with serotype‐2 dengue fever (i.e., rapid YES or NO diagnosis prepared for large populations, in terms of global public health). Paper‐based ELISA (specific to serotype‐2 dengue fever), which builds off of our previous studies and a revised previous ELISA procedure, owns multiple advantages: 1) high sensitivity (about 40 times higher than the current ELISA‐based approaches, due to our therapeutic‐based monoclonal antibody) and specificity (specific to dengue virus serotype‐2 nonstructural protein‐1 antigens); 2) tiny amount of sample and reagent used for single tests; 3) short operating duration (i.e., rapid diagnostic device); and, 4) inexpensiveness (appropriate for use in all developing and underdeveloped nations of the world). Due to the higher sensitivity and shorter operating duration of paper‐based ELISA (compared with conventional ELISA, and lateral flow immunoassays also performed in this study), this study has not only been able to perform the diagnosis of dengue virus serotype‐2 nonstructural protein‐1 antigens in both buffer system and human serum but also to evaluate dengue virus serotype‐2 envelope proteins in the buffer system, thus successfully achieving the first such use of these proteins as the target antigen for the development of diagnostic tools. These results provide a more comprehensive understanding for the genesis of dengue fever diagnostic tools (through antibody‐antigen recognition).
Intestinal perforation in a patient with severe ankylosing spondylitis
Authors: D N. Leitch, J N Fordham
Journal: Annals of the Rheumatic Diseases (1997)

Case historyA 54 year old man who had suVered from predominantly axial ankylosing spondylitis for 25 years was referred to see a gastroenterologist because of pallor in 1983.He was found to be anaemic, haemoglobin (Hb) 7.7 g/dl (13-18), mean cell volume (MCV) 57 fl (78-98), mean corpuscular haemoglobin (MCV) 17.5 pg (27.5-32.5),ferritin 27 µg/l (41-480), B12 and folate within normal limits, and to have a raised plasma viscosity 2.17 cps (1.5-1.72).He was taking indomethacin 25 mg thrice daily.Upper gastrointestinal endoscopy and barium enema were normal.The small bowel was not visualised and despite a microcytic hypochromic picture an anaemia of chronic disease was diagnosed.The haemoglobin had subsequently returned towards normal limits, Hb 10.3 g/dl, MCV 66 fl, MCH 20.3 pg, and ferritin 58 µg/l, when reviewed one year later.At the age of 60 years the patient attended the rheumatology department for the first time.Severe, predominantly axial, ankylosing spondylitis was noted with no lumbar spine movement and only 1 cm of chest expansion.Ranitidine 150 mg twice daily was added to the indomethacin for empirical gastrointestinal protection.At the age of 63 years the patient underwent a C2-C6 laminectomy for severe upper limb parasthesia.Later that year he was admitted as a general medical patient with suspected melaena with Hb 10.6 g/dl, MCV 75 fl (folate, B12, iron, and total iron binding capacity values were not recorded).A barium swallow was normal.Misoprostol was started in place of the ranitidine.The patient was advised to discontinue the indomethacin.However, because of good symptomatic relief this advice was not taken.One year later, at the age of 64 years the patient was again admitted to a general medical ward with suspected melaena, Hb 10.2 g/dl, MCV 66.7 fl.Upper gastrointestinal endoscopy was normal.It was assumed that the suspected melaena was secondary to non-steroidal anti-inflammatory drug (NSAID) use despite normal endoscopy, and that the anaemia was also a consequence of the chronic severe disease.A left total hip replacement was also carried out that year.
Antiperinuclear factors are present in polyarthritis before ACR criteria for rheumatoid arthritis are fulfilled
Authors: J.-M. Berthelot, Y. Maugars, A. Castagne, M. Audrain, A. Prost
Journal: Annals of the Rheumatic Diseases (1997)

To show that antiperinuclear factor (APF) may be useful for the diagnosis of rheumatoid arthritis at a time when the American College of Rheumatology (ACR) criteria are not yet fulfilled.Testing for APF-IgG (1:100 threshold) and rheumatoid factors (RF) was done in 60 patients with polyarthritis of recent onset during a three year follow up.At the end of the study, 21/40 rheumatoid arthritis were positive for RF and 31/40 for APF, including 18/40 cases (45%) in which ACR criteria were not yet fulfilled.APF are useful in the diagnosis of early rheumatoid arthritis.
Truncated DNMT3B Isoform DNMT3B7 Suppresses Growth, Induces Differentiation, and Alters DNA Methylation in Human Neuroblastoma
Authors: Kelly R. Ostler, Qiwei Yang, Timothy J. Looney, Li Zhang, Aparna Vasanthakumar, Yufeng Tian, Masha Kocherginsky, Stacey L. Raimondi, Jessica G. DeMaio, Helen R. Salwen, Song Gu, Alexandre Chlenski, Arlene Naranjo, Amy Gill, Radhika Peddinti, Bruce T. Lahn, Susan L. Cohn, Lucy A. Godley
Journal: Cancer Research (2012)

Epigenetic changes in pediatric neuroblastoma may contribute to the aggressive pathophysiology of this disease, but little is known about the basis for such changes. In this study, we examined a role for the DNA methyltransferase DNMT3B, in particular, the truncated isoform DNMT3B7, which is generated frequently in cancer. To investigate if aberrant DNMT3B transcripts alter DNA methylation, gene expression, and phenotypic character in neuroblastoma, we measured DNMT3B expression in primary tumors. Higher levels of DNMT3B7 were detected in differentiated ganglioneuroblastomas compared to undifferentiated neuroblastomas, suggesting that expression of DNMT3B7 may induce a less aggressive clinical phenotype. To test this hypothesis, we investigated the effects of enforced DNMT3B7 expression in neuroblastoma cells, finding a significant inhibition of cell proliferation in vitro and angiogenesis and tumor growth in vivo. DNMT3B7-positive cells had higher levels of total genomic methylation and a dramatic decrease in expression of the FOS and JUN family members that comprise AP1 transcription factors. Consistent with an established antagonistic relationship between AP1 expression and retinoic acid receptor activity, increased differentiation was seen in the DNMT3B7-expressing neuroblastoma cells following treatment with all-trans retinoic acid (ATRA) compared to controls. Our results indicate that DNMT3B7 modifies the epigenome in neuroblastoma cells to induce changes in gene expression, inhibit tumor growth, and increase sensitivity to ATRA.
In hemodialysis patients with CHF, adding telmisartan to standard ACE inhibitors reduced CHD mortality and admissions
Authors: Reem Mustafa, Amit X. Garg
Journal: Annals of Internal Medicine (2011)

Source CitationCice G, Di Benedetto A, D'Isa S, et al. Effects of telmisartan added to angiotensin-converting enzyme inhibitors on mortality and morbidity in hemodialysis patients with chronic heart failure: a double-blind, placebo-controlled trial. J Am Coll Cardiol. 2010;56:1701-8. https://pubmed.ncbi.nlm.nih.gov/21070920/
OLIG2 (BHLHB1), a bHLH Transcription Factor, Contributes to Leukemogenesis in Concert with LMO1
Authors: Ying-Wei Lin, Ramona Deveney, Mary Barbara, Norman N. Iscove, Stephen D. Nimer, Christopher Slape, Peter D. Aplan
Journal: Cancer Research (2005)

Abstract OLIG2 (originally designated BHLHB1) encodes a transcription factor that contains the basic helix-loop-helix motif. Although expression of OLIG2 is normally restricted to neural tissues, overexpression of OLIG2 has been shown in patients with precursor T-cell lymphoblastic lymphoma/leukemia (pre-T LBL). In the current study, we found that overexpression of OLIG2 was not only found in oligodendroglioma samples and normal neural tissue but also in a wide spectrum of malignant cell lines including leukemia, non–small cell lung carcinoma, melanoma, and breast cancer cell lines. To investigate whether enforced expression of OLIG2 is oncogenic, we generated transgenic mice that overexpressed OLIG2 in the thymus. Ectopic OLIG2 expression in the thymus was only weakly oncogenic as only 2 of 85 mice developed pre-T LBL. However, almost 60% of transgenic mice that overexpressed both OLIG2 and LMO1 developed pre-T LBL with large thymic tumor masses. Gene expression profiling of thymic tumors that developed in OLIG2/LMO1 mice revealed up-regulation of Notch1 as well as Deltex1 (Dtx1) and pre T-cell antigen receptor α (Ptcra), two genes that are considered to be downstream of Notch1. Of note, we found mutations in the Notch1 heterodimerization or proline-, glutamic acid-, serine-, and threonine-rich domain in three of six primary thymic tumors. In addition, growth of leukemic cell lines established from OLIG2/LMO1 transgenic mice was suppressed by a γ-secretase inhibitor, suggesting that Notch1 up-regulation is important for the proliferation of OLIG2-LMO1 leukemic cells.
Expression of Cysteinyl Leukotriene Receptors by CD34+ Umbilical Cord Blood (CB) - Progenitor Cells: Relevance to Atopic Development
Authors: J.A. Roa, A.J. Baatjes, L.D. Saleh, M.M. Cyr, G.M. Gauvreau, J.A. Denburg
Journal: Journal of Allergy and Clinical Immunology (2006)
Landmark article July 7, 1962: The battered-child syndrome. By C. Henry Kempe, Frederic N. Silverman, Brandt F. Steele, William Droegemueller, and Henry K. Silver
Authors: C. H. Kempe
Journal: JAMA (1984)

The battered-child syndrome, a clinical condition in young children who have received serious physical abuse, is a frequent cause of permanent injury or death. The syndrome should be considered in any child exhibiting evidence of fracture of any bone, subdural hematoma, failure to thrive, soft tissue swellings or skin bruising, in any child who dies suddenly, or where the degree and type of injury is at variance with the history given regarding the occurrence of the trauma. Psychiatric factors are probably of prime importance in the pathogenesis of the disorder, but knowledge of these factors is limited. Physicians have a duty and responsibility to the child to require a full evaluation of the problem and to guarantee that no expected repetition of trauma will be permitted to occur.
Adjuvant Chemotherapy for Lung Cancer: Cisplatin Doublets Only?
Authors: Daniel Morgensztern, Ramaswamy Govindan
Journal: Journal of the National Comprehensive Cancer Network (2008)

Lung cancer is the leading cause of cancer-related mortality worldwide. Despite adequate resection, more than half of patients die of recurrent disease, usually at distant sites. Adjuvant systemic chemotherapy is mainly used to eradicate micrometastatic disease. Since the seminal 1995 meta-analysis from earlier studies showed a trend toward improved survival with the use of cisplatin-based adjuvant chemotherapy, several randomized prospective adjuvant trials have addressed this question and eventually established the role for platinum-based adjuvant chemotherapy in patients with stage II or IIIA non-small cell lung cancer who have undergone complete resection. The role of adjuvant chemotherapy in patients with stage I disease remains controversial. Although no clinical or molecular predictors of recurrent disease after surgical resection are reliable, encouraging preliminary data on gene expression studies suggest that identifying, and perhaps treating, only patients at high risk for relapse might be possible in the near future. Furthermore, molecular predictors of resistance may guide the selection of chemotherapy in this setting.
Recommendations for Obesity Clinical Trials in Cancer Survivors: American Society of Clinical Oncology Statement
Authors: Jennifer A. Ligibel, Catherine M. Alfano, Dawn Hershman, Rachel M. Ballard, Suanna S. Bruinooge, Kerry S. Courneya, Elvan C. Daniels, Wendy Demark-Wahnefried, Elizabeth S. Frank, Pamela J. Goodwin, Melinda L. Irwin, Laura A. Levit, Worta McCaskill-Stevens, Lori M. Minasian, Mark A. O'Rourke, John P. Pierce, Kevin D. Stein, Cynthia A. Thomson, Clifford A. Hudis
Journal: Journal of Clinical Oncology (2015)

Observational evidence has established a relationship between obesity and cancer risk and outcomes. Interventional studies have demonstrated the feasibility and benefits of lifestyle change after cancer diagnosis, and guidelines recommend weight management and regular physical activity in cancer survivors; however, lifestyle interventions are not a routine part of cancer care. The ASCO Research Summit on Advancing Obesity Clinical Trials in Cancer Survivors sought to identify the knowledge gaps that clinical trials addressing energy balance factors in cancer survivors have not answered and to develop a roadmap for the design and implementation of studies with the potential to generate data that could lead to the evidence-based incorporation of weight management and physical activity programs into standard oncology practice. Recommendations highlight the need for large-scale trials evaluating the impact of energy balance interventions on cancer outcomes, as well as the concurrent conduct of studies focused on dissemination and implementation of interventions in diverse populations of cancer survivors, including answering critical questions about the degree of benefit in key subgroups of survivors. Other considerations include the importance of incorporating economic metrics into energy balance intervention trials, the need to establish intermediate biomarkers, and the importance of integrating traditional and nontraditional funding sources. Establishing lifestyle change after cancer diagnosis as a routine part of cancer care will require a multipronged effort to overcome barriers related to study development, funding, and stakeholder engagement. Given the prevalence of obesity and inactivity in cancer survivors in the United States and elsewhere, energy balance interventions hold the potential to reduce cancer morbidity and mortality in millions of patients, and it is essential that we move forward in determining their role in cancer care with the same care and precision used to test pharmacologic and other interventions.
Impaired basolateral sorting of pro-EGF causes isolated recessive renal hypomagnesemia
Authors: Wouter M. Tiel Groenestege, Stéphanie Thébault, Jenny van der Wijst, Dennis van den Berg, Rob Janssen, Sabine Tejpar, Lambertus P. van den Heuvel, Eric van Cutsem, Joost G. Hoenderop, Nine V. Knoers, René J. Bindels
Journal: Journal of Clinical Investigation (2007)

Primary hypomagnesemia constitutes a rare heterogeneous group of disorders characterized by renal or intestinal magnesium (Mg2+) wasting resulting in generally shared symptoms of Mg2+ depletion, such as tetany and generalized convulsions, and often including associated disturbances in calcium excretion. However, most of the genes involved in the physiology of Mg2+ handling are unknown. Through the discovery of a mutation in the EGF gene in isolated autosomal recessive renal hypomagnesemia, we have, for what we believe is the first time, identified a magnesiotropic hormone crucial for total body Mg2+ balance. The mutation leads to impaired basolateral sorting of pro-EGF. As a consequence, the renal EGFR is inadequately stimulated, resulting in insufficient activation of the epithelial Mg2+ channel TRPM6 (transient receptor potential cation channel, subfamily M, member 6) and thereby Mg2+ loss. Furthermore, we show that colorectal cancer patients treated with cetuximab, an antagonist of the EGFR, develop hypomagnesemia, emphasizing the significance of EGF in maintaining Mg2+ balance.
Predictors of response to tiotropium versus salmeterol in asthmatic adults
Authors: Stephen P. Peters, Eugene R. Bleecker, Susan J. Kunselman, Nikolina Icitovic, Wendy C. Moore, Rodolfo Pascual, Bill T. Ameredes, Homer A. Boushey, William J. Calhoun, Mario Castro, Reuben M. Cherniack, Timothy Craig, Loren C. Denlinger, Linda L. Engle, Emily A. DiMango, Elliot Israel, Monica Kraft, Stephen C. Lazarus, Robert F. Lemanske, Njira Lugogo, Richard J. Martin, Deborah A. Meyers, Joe Ramsdell, Christine A. Sorkness, E. Rand Sutherland, Stephen I. Wasserman, Michael J. Walter, Michael E. Wechsler, Vernon M. Chinchilli, Stanley J. Szefler
Journal: Journal of Allergy and Clinical Immunology (2013)
Benzodiazepine-induced superoxide signalsB cell apoptosis: mechanistic insight and potential therapeutic utility
Authors: Neal B. Blatt, Jeffrey J. Bednarski, Roscoe E. Warner, Francesco Leonetti, Kathryn M. Johnson, Anthony Boitano, Raymond Yung, Bruce C. Richardson, Kent J. Johnson, Jonathan A. Ellman, Anthony W. Opipari, Gary D. Glick
Journal: Journal of Clinical Investigation (2002)

The properties of a proapoptotic 1,4-benzodiazepine, Bz-423, identified through combinatorial chemistry and phenotype screening are described. Bz-423 rapidly generated superoxide (O2–) in transformed Ramos B cells. This O2– response originated from mitochondria prior to mitochondrial transmembrane gradient collapse and opening of the permeability transition pore. Bz-423–induced O2– functioned as an upstream signal that initiated an apoptotic program characterized by cytochrome c release, mitochondrial depolarization, and caspase activation. Pretreatment of cells with agents that either block the formation of Bz-423–induced O2– or scavenge free radicals attenuated the death cascade, which demonstrated that cell killing by Bz-423 depends on O2–. Parallels between Ramos cells and germinal center B cells prompted experiments to determine whether Bz-423 had therapeutic activity in vivo. This possibility was tested using the (NZB × NZW)F1 murine model of lupus, in which the pathologically enhanced survival and expansion of germinal center B cells mediate disease. Administration of Bz-423 for 12 weeks specifically controlled germinal center hyperplasia and reduced the histological evidence of glomerulonephritis. Collectively, these studies define a new structure-function relationship for benzodiazepines and point to a new target and mechanism that could be of value for developing improved drugs to manage systemic lupus erythematosus and related disorders.
Pneumothorax following thoracic radiation therapy for Hodgkin's disease.
Authors: M G Penniment, P C O'Brien
Journal: Thorax (1994)

Radiation therapy alone to the nodal drainage sites above the diaphragm, namely a "mantle" field, is often standard treatment for early stage Hodgkin9s disease and may be used in combination with chemotherapy in more advance disease. Localised pneumonitis and fibrosis are recognised treatment related sequelae; however, other pulmonary complications, including pneumothorax, have been described. Two cases of spontaneous pneumothorax following mantle radiation therapy are presented.
Host Lymphodepletion Augments T Cell Adoptive Immunotherapy through Enhanced Intratumoral Proliferation of Effector Cells
Authors: Li-Xin Wang, Suyu Shu, Gregory E. Plautz
Journal: Cancer Research (2005)

Abstract T-cell adoptive immunotherapy for stringent murine tumor models, such as intracranial, s.c., or advanced pulmonary metastases, routinely uses lymphodepletive conditioning regimens before T-cell transfer, like recent clinical protocols. In this study, we examined whether host lymphodepletion is an obligatory component of curative T-cell therapy; we also examined the mechanism by which it augments therapy. Mice bearing intracranial, s.c., or 10-day pulmonary metastases of MCA 205 received total body irradiation conditioning or were nonirradiated before i.v. transfer of tumor-reactive T cells. Total body irradiation was not required for immunologically specific curative therapy and induction of memory provided that a 3- to 12-fold higher T-cell dose was administered. The mechanism involved enhanced intratumoral proliferation of T-effector cells in total body irradiation–conditioned recipients. In this tumor model, intratumoral Treg cells were not detected; consequently, intratumoral T-effector cells produced identical amounts of IFN-γ upon ex vivo antigen stimulation irrespective of total body irradiation conditioning. Thus, host lymphodepletion augments T-cell immunotherapy through enhanced antigen-driven proliferation of T-effector cells, but curative therapy can be achieved in nonconditioned hosts by escalation of T-cell dose. These data provide a rationale for dose escalation of T-effector cells in situations where single or repeated lymphodepletion regimens are contraindicated.
Cisplatin-Based Adjuvant Chemotherapy in Patients with Completely Resected Non–Small-Cell Lung Cancer
Authors: Rodrigo Arriagada, Bengt Bergman, Ariane Dunant, Thierry Le Chevalier, Jean-Pierre Pignon, Johan Vansteenkiste
Journal: New England Journal of Medicine (2004)

On the basis of a previous meta-analysis, the International Adjuvant Lung Cancer Trial was designed to evaluate the effect of cisplatin-based adjuvant chemotherapy on survival after complete resection of non–small-cell lung cancer.
Randomised study of antiepileptic drug withdrawal in patients in remission
Authors: P. Bessant, D. Chadwick, B. Eaton, J. Taylor, A. Holland, J. Joannou, A.L. Johnson, L. Oldfield, N.P. Reader, E.J.W. Gumpert, A. Jacoby, H. Cuckle, C. Warlow
Journal: The Lancet (1991)
Dose-Intense Taxol: High Response Rate in Patients With Platinum-Resistant Recurrent Ovarian Cancer
Authors: E. C. Kohn, G. Sarosy, A. Bicher, C. Link, M. Christian, S. M. Steinberg, M. Rothenberg, D. O. Adamo, P. Davis, F. P. Ognibene, R. E. Cunnion, E. Reed
Journal: JNCI Journal of the National Cancer Institute (1994)

Paclitaxel (Taxol), a diterpene plant product that promotes tubulin polymerization, has documented activity against a number of solid tumors, including ovarian cancer and breast cancer Our purpose was to conduct a phase II clinical trial investigating the response of patients with advanced recurrent ovarian carcinoma to high-dose paclitaxel combined with gran-ulocyte colony-stimulating factor (G-CSF) A prospective phase II clinical trial of patients with advanced-stage, recurrent ovarian cancer was undertaken. Patients received 250 mg/m2 paclitaxel every 21 days; cycles were given on a rigid schedule; delays were permitted only for extreme circumstances. G-CSF at a dose of 10 p-g/kg per day was given to ameliorate myelo-suppression. If a patient showed fever and neutropenia, G-CSF dosage was increased to 20 μg/kg per day so that paclitaxel dose intensity could be maintained. Patients were assessed for response every two cycles, and those with complete radiographic resolution of disease underwent peritoneoscopy. Forty-four patients were assessable for response. Twenty-one had a reduction in tumor volume greater than 50%, yielding an objective response rate of 48% (21 of 44 patients; 95% confidence interval, 32%-63%). Six (14%) of the 44 patients had complete radiographic resolution of disease; two of the six also had negative biopsy specimens and washings at peritoneoscopy. Age, number of prior regimens, and clinical platinum resistance did not influence response rate or ability to maintain dose intensity. Dose intensity was maintained at the targeted level for up to 14 consecutive cycles of therapy. We observed a 48% response rate with dose-intense paclitaxel for patients with advanced-stage, platinum-resistant, recurrent ovarian cancer. The response rate is higher than previously reported for paclitaxel at a lower dose in similar cohorts of patients treated without G-CSF. Comparison of phase II studies of paclitaxel suggests a dose-response relationship. Therapy with dose-intense paclitaxel and G-CSF should be considered for patients with advanced, platinum-refractory ovarian cancer. [J Natl Cancer Inst 86:18–24, 1994]