tbuckley/cabot-search huggingface dataset:
Electromagnetic Interference From Radio Frequency Identification Inducing Potentially Hazardous Incidents in Critical Care Medical Equipment
Authors: Remko van der Togt
Journal: JAMA (2008)

Health care applications of autoidentification technologies, such as radio frequency identification (RFID), have been proposed to improve patient safety and also the tracking and tracing of medical equipment. However, electromagnetic interference (EMI) by RFID on medical devices has never been reported.To assess and classify incidents of EMI by RFID on critical care equipment.Without a patient being connected, EMI by 2 RFID systems (active 125 kHz and passive 868 MHz) was assessed under controlled conditions during May 2006, in the proximity of 41 medical devices (in 17 categories, 22 different manufacturers) at the Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands. Assessment took place according to an international test protocol. Incidents of EMI were classified according to a critical care adverse events scale as hazardous, significant, or light.In 123 EMI tests (3 per medical device), RFID induced 34 EMI incidents: 22 were classified as hazardous, 2 as significant, and 10 as light. The passive 868-MHz RFID signal induced a higher number of incidents (26 incidents in 41 EMI tests; 63%) compared with the active 125-kHz RFID signal (8 incidents in 41 EMI tests; 20%); difference 44% (95% confidence interval, 27%-53%; P < .001). The passive 868-MHz RFID signal induced EMI in 26 medical devices, including 8 that were also affected by the active 125-kHz RFID signal (26 in 41 devices; 63%). The median distance between the RFID reader and the medical device in all EMI incidents was 30 cm (range, 0.1-600 cm).In a controlled nonclinical setting, RFID induced potentially hazardous incidents in medical devices. Implementation of RFID in the critical care environment should require on-site EMI tests and updates of international standards.
Hemorrhagic Bullae in Gonococcemia
Authors: A. Bernard Ackerman
Journal: New England Journal of Medicine (1970)

CHARACTERISTIC cutaneous lesions can be the clue to the diagnosis of gonococcal septicemia. Frequently, these sparse, acral lesions occurring in young adults, especially women, who have fever, polyarthralgia, and tenosynovitis, are dismissed as folliculitis or regarded as manifestations of "flu," acute rheumatic fever or systemic lupus erythematosus. The skin lesions of gonococcemia are "virtually specific."1 Heralded by "splinter-like" pain, the fully developed lesions have been emphasized as being of two types: purpuric and vesiculopustular on broad erythematous bases.2 , 3 A third variant, hemorrhagic bullae, has not been described since the advent of antibiotics.4 The most prominent skin lesions in two recently . . .
Antigenic liposomes displaying CD22 ligands induce antigen-specific B cell apoptosis
Authors: Matthew S. Macauley, Fabian Pfrengle, Christoph Rademacher, Corwin M. Nycholat, Andrew J. Gale, Annette von Drygalski, James C. Paulson
Journal: Journal of Clinical Investigation (2013)

Antibodies confer humoral immunity but can also be harmful when they target an autoantigen, alloantigen, allergen, or biotherapeutic. New strategies are needed for antigen-specific suppression of undesired antibody responses, particularly to T cell-dependent protein antigens, because they elicit T cell help. Here we show that liposomal nanoparticles, displaying both antigen and glycan ligands of the inhibitory coreceptor CD22, induce a tolerogenic program that selectively causes apoptosis in mouse and human B cells. These SIGLEC-engaging tolerance-inducing antigenic liposomes (STALs, where SIGLEC is defined as sialic acid-binding Ig-like lectin) induced robust antigen-specific tolerance to protein antigens in mice, preventing subsequent immune response to challenge with the same antigen. Since development of inhibitory antibodies to FVIII is a serious problem in treatment of hemophilia A patients, we investigated the potential of this approach for inducing tolerance to FVIII in a hemophilia mouse model. STALs prevented formation of inhibitory FVIII antibodies, allowing for effective administration of FVIII to hemophilia mice to prevent bleeding. These findings suggest that STALs could be used to eliminate or prevent harmful B cell-mediated immune responses.
Surfactant Homeostasis Is Maintained <i>In Vivo</i> during Keratinocyte Growth Factor–induced Rat Lung Type II Cell Hyperplasia
Authors: Antonia Fehrenbach, Christoph Bube, Jens M. Hohlfeld, Paul Stevens, Thomas Tschernig, Heinz G. Hoymann, Norbert Krug, Heinz Fehrenbach
Journal: American Journal of Respiratory and Critical Care Medicine (2003)

Keratinocyte growth factor (KGF) induces transient proliferation of alveolar type II cells (AEII) associated with surfactant alterations. To test the hypothesis that homeostasis of intracellular phospholipid stores is maintained under KGF-induced hyperplasia, we (1) collected tissue from adult rat lungs, fixed for light and electron microscopy 3 days after intratracheal instillation of 5 mg recombinant human (rHu) KGF/kg body weight or phosphate-buffered saline (PBS), and from untreated control animals (five animals/group) for design-based stereology of AEII and lamellar body (LB) ultrastructure; and (2) we analyzed uptake and distribution of instilled radiolabeled phospholipids. After rHuKGF, AEII-coverage of alveolar walls (PBS:8.3 +/- 3.0%; rHuKGF:30.6 +/- 4.8%) and number of AEII/ml lung volume (PBS:28.5 +/- 6.5 x 10(6); rHuKGF:48.2 +/- 5.8 x 10(6)) were increased (p < 0.008). Number (PBS:97 +/- 25; rHuKGF:54 +/- 7) and volume (PBS:45.3 +/- 13.8 microm(3); rHuKGF:21.0 +/- 4.7 microm(3)) of LBs per cell were decreased (p < 0.008), but not total amount/ml lung volume (PBS:128 +/- 46. 4 x 10(7) microm(3); rHuKGF:103 +/- 34. 7 x 10(7) microm(3)). This was paralleled by a shift to larger LBs. After rHuKGF, radiolabeled phospholipids accumulated in whole lung tissue relative to lavage fluid (p < 0.01). However, less radiolabel was incorporated per cell (p < 0.01). We conclude that under rHuKGF-induced AEII proliferation intracellular surfactant was decreased per single cell, whereas a constant amount was maintained per unit lung volume. We suggest that surfactant homeostasis is regulated at the level of phospholipid transport processes, for example, secretion and reuptake.
Concentrations of pyridinoline and deoxypyridinoline in joint tissues from patients with osteoarthritis or rheumatoid arthritis.
Authors: M Takahashi, K Kushida, H Hoshino, M Suzuki, M Sano, S Miyamoto, T Inoue
Journal: Annals of the Rheumatic Diseases (1996)

OBJECTIVE: To assess the usefulness of pyridinoline (Pyr) and deoxypyridinoline (Dpyr), intermolecular crosslinks of collagen, as markers in the evaluation of arthritis, by studying their distribution in tissues from knee joints. METHODS: Joint tissues (cartilage, bone, synovium) were obtained during operation from 10 patients with osteoarthritis (OA) and 10 patients with rheumatoid arthritis (RA). Synovium was also obtained from 10 non-arthritic (NA) subjects. Hydroxyproline was measured in hydrolysed tissue samples and converted to an equivalent collagen content. The amounts of Pyr and Dpyr crosslinks measured in the hydrolysed samples using a fluorescence technique were expressed as mumol/mol of collagen. RESULTS: Pyr and Dpyr were distributed in all three tissues, but in different amounts. The ratio of the contents of Pyr and (Pyr:Dpyr) was 50:1 in cartilage, 3:1 in bone, and 25:1 in synovium. OA cartilage had a greater Dpyr content than the RA cartilage, but there was no other significant difference in the contents of Pyr and Dpyr and the ratio Pyr:Dpyr in the joint tissues from patients with OA or RA. In synovium, there was no significant difference between the contents of Pyr and Dpyr and the Pyr:Dpyr ratio among OA, RA, and NA tissues. CONCLUSION: Both Pyr and Dpyr were located in cartilage, bone, and synovium. A significant amount of Pyr and Dpyr in these joint tissues, especially in synovium, may contribute to the urinary excretion of those crosslinks that is observed in arthritis.
Overexpression of Vascular Endothelial Growth Factor-B in Mouse Heart Alters Cardiac Lipid Metabolism and Induces Myocardial Hypertrophy
Authors: Terhi Karpanen, Maija Bry, Hanna M. Ollila, Tuulikki Seppänen-Laakso, Erkki Liimatta, Hanna Leskinen, Riikka Kivelä, Teemu Helkamaa, Mari Merentie, Michael Jeltsch, Karri Paavonen, Leif C. Andersson, Eero Mervaala, Ilmo E. Hassinen, Seppo Ylä-Herttuala, Matej Orešič, Kari Alitalo
Journal: Circulation Research (2008)

Vascular endothelial growth factor (VEGF)-B is poorly angiogenic but prominently expressed in metabolically highly active tissues, including the heart. We produced mice expressing a cardiac-specific VEGF-B transgene via the alpha-myosin heavy chain promoter. Surprisingly, the hearts of the VEGF-B transgenic mice showed concentric cardiac hypertrophy without significant changes in heart function. The cardiac hypertrophy was attributable to an increased size of the cardiomyocytes. Blood capillary size was increased, whereas the number of blood vessels per cell nucleus remained unchanged. Despite the cardiac hypertrophy, the transgenic mice had lower heart rate and blood pressure than their littermates, and they responded similarly to angiotensin II-induced hypertension, confirming that the hypertrophy does not compromise heart function. Interestingly, the isolated transgenic hearts had less cardiomyocyte damage after ischemia. Significantly increased ceramide and decreased triglyceride levels were found in the transgenic hearts. This was associated with structural changes and eventual lysis of mitochondria, resulting in accumulation of intracellular vacuoles in cardiomyocytes and increased death of the transgenic mice, apparently because of mitochondrial lipotoxicity in the heart. These results suggest that VEGF-B regulates lipid metabolism, an unexpected function for an angiogenic growth factor.
Oral doxycycline versus intravenous ceftriaxone for European Lyme neuroborreliosis: a multicentre, non-inferiority, double-blind, randomised trial
Authors: Unn Ljøstad, Eirik Skogvoll, Randi Eikeland, Rune Midgard, Tone Skarpaas, Åse Berg, Åse Mygland
Journal: The Lancet Neurology (2008)
Involvement of CXCR4 and IL-2 in the homing and retention of human NK and NK T cells to the bone marrow and spleen of NOD/SCID mice
Authors: Katia Beider, Arnon Nagler, Ori Wald, Suzanna Franitza, Michal Dagan-Berger, Hanna Wald, Hilla Giladi, Stefan Brocke, Jacob Hanna, Ofer Mandelboim, Merav Darash-Yahana, Eithan Galun, Amnon Peled
Journal: Blood (2003)
A Phase I/II Clinical Trial in Localized Prostate Cancer of an Adenovirus Expressing Nitroreductase with CB1984
Authors: Prashant Patel, J Graham Young, Vivien Mautner, Daniel Ashdown, Sarah Bonney, Robert G Pineda, Stuart I Collins, Peter F Searle, Diana Hull, Elizabeth Peers, John Chester, D Michael Wallace, Alan Doherty, Hing Leung, Lawrence S Young, Nicholas D James
Journal: Molecular Therapy (2009)

We report a phase I/II clinical trial in prostate cancer (PCa) using direct intraprostatic injection of a replication defective adenovirus vector (CTL102) encoding bacterial nitroreductase (NTR) in conjunction with systemic prodrug CB1954. One group of patients with localized PCa scheduled for radical prostatectomy received virus alone, prior to surgery, in a dose escalation to establish safety, tolerability, and NTR expression. A second group with local failure following primary treatment received virus plus prodrug to establish safety and tolerability. Based on acceptable safety data and indications of prostate-specific antigen (PSA) responses, an extended cohort received virus at a single dose level plus prodrug. The vector was well tolerated with minimal side effects, had a short half-life in the circulation, and stimulated a robust antibody response. Immunohistochemistry of resected prostate demonstrated NTR staining in tumor and glandular epithelium at all dose levels [5 × 1010–1 × 1012 virus particles (vp)]. A total of 19 patients received virus plus prodrug and 14 of these had a repeat treatment; minimal toxicity was observed and there was preliminary evidence of change in PSA kinetics, with an increase in the time to 10% PSA progression in 6 out of 18 patients at 6 months. We report a phase I/II clinical trial in prostate cancer (PCa) using direct intraprostatic injection of a replication defective adenovirus vector (CTL102) encoding bacterial nitroreductase (NTR) in conjunction with systemic prodrug CB1954. One group of patients with localized PCa scheduled for radical prostatectomy received virus alone, prior to surgery, in a dose escalation to establish safety, tolerability, and NTR expression. A second group with local failure following primary treatment received virus plus prodrug to establish safety and tolerability. Based on acceptable safety data and indications of prostate-specific antigen (PSA) responses, an extended cohort received virus at a single dose level plus prodrug. The vector was well tolerated with minimal side effects, had a short half-life in the circulation, and stimulated a robust antibody response. Immunohistochemistry of resected prostate demonstrated NTR staining in tumor and glandular epithelium at all dose levels [5 × 1010–1 × 1012 virus particles (vp)]. A total of 19 patients received virus plus prodrug and 14 of these had a repeat treatment; minimal toxicity was observed and there was preliminary evidence of change in PSA kinetics, with an increase in the time to 10% PSA progression in 6 out of 18 patients at 6 months.
MB-06 * PROGNOSTIC IMPACT OF O6-METHYLGUANINE-DNA METHYLTRANSFERASE (MGMT) PROMOTER METHYLATION IN MEDULLOBLASTOMA
Authors: A. Kondo, T. Kurimoto, S. Sakaguchi, H. Arai
Journal: Neuro-Oncology (2015)

BACKGROUND: O6-methylguanine-DNA methyltransferase (MGMT) is a DNA repair enzyme that plays an important role in tumor resistance to alkylating agents. Recent study revealed that MGMT promoter methylation is associated with favorable outcomes in malignant glioma patients. However, MGMT status in pediatric medulloblastoma and the prognostic impact of this methylation status and clinical outcomes of this tumor has not been fully evaluated. The objective of this study is to investigate the association between MGMT methylation status and clinical outcomes for medulloblastoma patients. MATERIALS AND METHODS: Patients with medulloblastoma treated at our institution between 1995 and 2012 were reviewed retrospectively. Tumor tissues were obtained from formalin-fixed paraffin-embedded tumor samples. Methylation statuses of 18 CpG sites of MGMT promoter region were determined by bisulfite sequencing analysis. RESULTS: Tumor material and clinical information were available for 22 patients. Median follow-up period was 48 months (13-190 months). Median age at diagnosis was 8.5 years (1-23 years). After the first line treatment, 10 had been in complete remission, 8 had relapse of disease, 1 had progressive disease, 1 had stable disease and 2 were lost follow-up. The patients in complete remission had higher accumulation of methylated CpG sites (median 5, range 2-9) than the relapsed patients (median 2, range 1-4) (p = 0.036). CONCLUSION: The results indicated that MGMT promoter methylation correlates with favorable outcome of medulloblastoma.
Shifts in the Therapeutic Paradigm for Patients Newly Diagnosed with Multiple Myeloma: Maintenance Therapy and Overall Survival
Authors: Antonio Palumbo, Michel Attal, Murielle Roussel
Journal: Clinical Cancer Research (2011)

Abstract High-dose therapy (HDT) with autologous stem cell transplantation (ASCT) is the standard of care for eligible newly diagnosed multiple myeloma (MM) patients. Several randomized studies showed a survival advantage for patients undergoing transplantation, compared with conventional chemotherapy. Introduction of new drugs in this setting has markedly increased survival rates within the last 10 years. Efforts to further improve response rates and survival in those patients are still needed, mainly by increasing the depth of tumor reduction and the duration of response through more effective induction, consolidation, and maintenance therapies. Nevertheless, this approach is currently challenged by the promising results of long-term treatment with novel agents. Recent data suggest that the upfront combination of a proteasome inhibitor plus 1 immunomodulatory compound (IMiD) is highly effective. The combination of bortezomib, thalidomide, and dexamethasone (VTD) has proven to be highly effective as a frontline treatment and is significantly superior to vincristine, doxorubicin, and dexamethasone (VAD) or thalidomide and dexamethasone (Thal-Dex) before and after ASCT with a very manageable toxicity pattern. The most promising 3-drug association might be bortezomib, lenalidomide, and dexamethasone (VRD). Adjunction of a 4th drug has not proven to be more efficient. In patients not eligible for ASCT, the introduction of novel agents has changed the management of multiple myeloma. The combinations of melphalan, prednisone, and thalidomide and of bortezomib, melphalan, and prednisone have shown improved progression-free survival and overall survival in comparison with melphalan and prednisone alone. Melphalan, prednisone, and thalidomide and bortezomib, melphalan, and prednisone are now the new standards of care for elderly patients. Preliminary results also support the role of the combination of melphalan, prednisone, and lenalidomide followed by maintenance therapy with lenalidomide in the treatment of elderly patients. Physicians now have a wider variety of treatment options to tailor the most appropriate and efficacious treatment according to their patients' characteristics. Clin Cancer Res; 17(6); 1253–63. ©2011 AACR.
Association Between Level of Hepatitis B Surface Antigen and Relapse After Entecavir Therapy for Chronic Hepatitis B Virus Infection
Authors: Chien-Hung Chen, Chao-Hung Hung, Tsung-Hui Hu, Jing-Houng Wang, Sheng-Nan Lu, Pei-Fang Su, Chuan-Mo Lee
Journal: Clinical Gastroenterology and Hepatology (2015)
Global Help for Post-Ebola Recovery in West Africa
Authors: M. J. Friedrich
Journal: JAMA (2015)

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Risk of suicide among users of calcium channel blockers: population based, nested case-control study
Authors: C. Gasse
Journal: BMJ (2000)

Lindberg et al reported the results of two studies, which they interpreted as showing that calcium channel blockers may increase the risk of suicide. 1 They found a significant correlation between rates of suicide and use of calcium channel blockers (r = 0.29, P < 0.001) in a cross sectional ecological study and an increased risk of suicide (relative risk 5.4, 95% confidence interval 1.4 to 20.5) in users of calcium channel blockers compared with non-users.But they did not control for important independent risk factors such as depression and did not validate diagnoses of suicide.We aimed at investigating further the possible association between use of calcium channel blockers and risk of suicide among people with hypertension, given the limitations of Lindberg et al's study.
Abnormal immune responses of Bloom's syndrome lymphocytes in vitro.
Authors: T H Hütteroth, S D Litwin, J German
Journal: Journal of Clinical Investigation (1975)

Bloom's syndrome is a rare autosmal recessive disorder, first characterized by growth retardation and asum-sensitive facial telangiectasia and more recently demonstarted to have increased chromosome instability, a predisposition to malignancy, and increased susecptibitily to infection. The present report ocncern the immune function of Bloom's syndrom lymphoctes in vitro. Four affected homozgotes and five heterozygotes were studied. An abnormal serum concentartion of at least one class of immunoglobin was present in three out of four homozgotes. Affected homozgotes were shown capable of both a humoral and cellular response after antigenic challenge, the responses in general being weak but detectable. Blood lymphocytes from Bloom's syndrome individuals were cultured in impaired proliferavite response and synthesized less immunoglobulin at the end of 5 days than did normal controls. In contrast, they had a normal proliferative response to phytohemagglutinin except at highest concentrations of the mitogen. In the mixed lymphocte culture, Bloom's syndrome lymphocytes proved to be poor responder cells but normal stimulator cells. Lmyphoctes from the heterozgotes produced normal responses in these three systems. Distrubed immunity appears to be on of several major consequences of homozygosity for the Bloom's syndrome gene. Although the explanation for this pleiotropism is at present obscure, the idea was advanced that the aberrant immune function is, along with the major clincial feature-small body size, amanifestation of defect in cellular proliferation.
Continuities Between Emotional and Disruptive Behavior Disorders in Adolescence and Personality Disorders in Adulthood
Authors: Margareth I. Helgeland, Ellen Kjelsberg, Svenn Torgersen
Journal: American Journal of Psychiatry (2005)

The purpose of this study was to quasiprospectively investigate continuities between emotional and disruptive behavior disorders in adolescence and personality disorders in adulthood.One hundred thirty subjects (age: mean=43.2 years) who had been diagnosed with emotional and disruptive behavior disorders during adolescence (age: mean=14.6 years) and rediagnosed based on hospital records, according to DSM-IV, were interviewed with the Structured Interview for DSM-IV Personality to establish whether they suffered from personality disorders at the 28-year follow-up.Adolescents with disruptive behavior disorders were not more likely to have personality disorders in adulthood than adolescents with emotional disorders. Adolescents with disruptive behavior disorders were significantly more likely to have cluster B personality disorders at follow-up than adolescents with emotional disorders. Logistic regression analyses revealed that disruptive behavior disorders in females were significantly more strongly associated with a high risk of cluster B diagnoses at follow-up than in males. Emotional disorders were significant and independent predictors of cluster C personality disorders in women but not in men. Disruptive behavior disorders were a significant and independent predictor of antisocial personality disorders in men.These results support the view that personality disorders can be traced back to adolescent emotional and disruptive behavior disorders. The moderating effect of gender in cluster B and cluster C personality disorders suggests that sociocultural and biological factors may contribute to different adult outcomes in men and women with similar adolescent psychiatric disorders.