tbuckley/cabot-search huggingface dataset:
Risk for Hospitalization With Depression After a Cancer Diagnosis: A Nationwide, Population-Based Study of Cancer Patients in Denmark From 1973 to 2003
Authors: Susanne O. Dalton, Thomas Munk Laursen, Lone Ross, Preben Bo Mortensen, Christoffer Johansen
Journal: Journal of Clinical Oncology (2009)

As more people survive cancer, it is necessary to understand the long-term impact of cancer. We investigated whether cancer survivors are at increased risk for hospitalization for depression.We linked data on all 5,703,754 persons living in Denmark on January 1, 1973, or born thereafter to the Danish Cancer Registry and identified 608,591 adults with a diagnosis of cancer. Follow-up for hospitalization for depression in the Danish Psychiatric Central Register from 1973 through 2003 yielded 121,227,396 person-years and 121,304 hospitalizations for depression. The relative risk (RR) for depression among cancer survivors relative to the cancer-free population was estimated by Poisson regression analysis with adjustment for age and period and stratified by sex, site of cancer, and extent of disease.The risk for depression in the first year after a cancer diagnosis was increased, with RRs ranging from 1.16 (95% CI, 0.90 to 1.51) in women with colorectal cancer to 3.08 (95% CI, 1.88 to 5.02) in men with brain cancer. Decreasing but still significant excess risks during subsequent years were observed for most specific cancers. The risk remained increased throughout the study period for both men and women surviving hormone-related cancers, for women surviving smoking-related cancers, and for men surviving virus- and immune-related cancers.This study confirms an increased risk for depression in patients facing a disruptive event like cancer. Early recognition and effective treatment are needed to prevent admission of cancer survivors for depression.
MHC class II–restricted antigen presentation by plasmacytoid dendritic cells inhibits T cell–mediated autoimmunity
Authors: Magali Irla, Natalia Küpfer, Tobias Suter, Rami Lissilaa, Mahdia Benkhoucha, Jonathan Skupsky, Patrice H. Lalive, Adriano Fontana, Walter Reith, Stéphanie Hugues
Journal: The Journal of Experimental Medicine (2010)

Although plasmacytoid dendritic cells (pDCs) express major histocompatibility complex class II (MHCII) molecules, and can capture, process, and present antigens (Ags), direct demonstrations that they function as professional Ag-presenting cells (APCs) in vivo during ongoing immune responses remain lacking. We demonstrate that mice exhibiting a selective abrogation of MHCII expression by pDCs develop exacerbated experimental autoimmune encephalomyelitis (EAE) as a consequence of enhanced priming of encephalitogenic CD4+ T cell responses in secondary lymphoid tissues. After EAE induction, pDCs are recruited to lymph nodes and establish MHCII-dependent myelin-Ag–specific contacts with CD4+ T cells. These interactions promote the selective expansion of myelin-Ag–specific natural regulatory T cells that dampen the autoimmune T cell response. pDCs thus function as APCs during the course of EAE and confer a natural protection against autoimmune disease development that is mediated directly by their ability to present of Ags to CD4+ T cells in vivo.
Pleurectomy in a 10 week old child to control staphylococcal associated pneumothoraces.
Authors: S Large, J Warner, P Goldstraw
Journal: Thorax (1984)

Staphylococcal pneumonia may be complicated by metas- tatic abscess, acute endocarditis, meningitis, bronchiec- tasis, osteomyelitis, pneumatocele, and pyo- pneumothorax.Staphylococcal pneumonia is a well recog- nised infection in paediatric practice and about 60% of cases occur in the first six months of life.Pneumatocele and
Combining PM <sub>2.5</sub> Component Data from Multiple Sources: Data Consistency and Characteristics Relevant to Epidemiological Analyses of Predicted Long-Term Exposures
Authors: Sun-Young Kim, Lianne Sheppard, Timothy V. Larson, Joel D. Kaufman, Sverre Vedal
Journal: Environmental Health Perspectives (2015)

Regulatory monitoring data have been the exposure data resource most commonly applied to studies of the association between long-term PM2.5 components and health. However, data collected for regulatory purposes may not be compatible with epidemiological studies.We studied three important features of the PM2.5 component monitoring data to determine whether it would be appropriate to combine all available data from multiple sources for developing spatiotemporal prediction models in the National Particle Component and Toxicity (NPACT) study.The NPACT monitoring data were collected in an extensive monitoring campaign targeting cohort participant residences. The regulatory monitoring data were obtained from the Chemical Speciation Network (CSN) and the Interagency Monitoring of Protected Visual Environments (IMPROVE). We performed exploratory analyses to examine features that could affect our approach to combining data: comprehensiveness of spatial coverage, comparability of analysis methods, and consistency in sampling protocols. In addition, we considered the viability of developing spatiotemporal prediction models given a) all available data, b) NPACT data only, and c) NPACT data with temporal trends estimated from other pollutants.The number of CSN/IMPROVE monitors was limited in all study areas. The different laboratory analysis methods and sampling protocols resulted in incompatible measurements between networks. Given these features we determined that it was preferable to develop our spatiotemporal models using only the NPACT data and under simplifying assumptions.Investigators conducting epidemiological studies of long-term PM2.5 components need to be mindful of the features of the monitoring data and incorporate this understanding into the design of their monitoring campaigns and the development of their exposure prediction models.
STUDIES ON THE MODE OF ACTION OF DIPHTHERIA TOXIN
Authors: Ronald S. Goor, A. M. Pappenheimer
Journal: The Journal of Experimental Medicine (1967)

The ability of a number of nucleotides related to NAD to replace NAD as cofactors for inhibition by diphtheria toxin of peptide bond formation has been examined. Neither NADH nor NADP are active. Of some 14 analogues closely related structurally to NAD that have been tested, only 3-thiocarboxamide pyridine-AD is as active as NAD itself. Replacement of the 3-carboxamide group on the pyridine ring by an acetyl group, or deamination of the purine ring, resulted in derivatives with reduced activity. The results were interpreted as suggesting that NAD and certain related nucleotides are capable of specific interaction with diphtheria toxin. Using the method of equilibrium dialysis, reversible binding of 1 mole of NAD per mole of toxin has been demonstrated. Toxoid does not interact with NAD.
Effects of an endurance cycling competition on resting serum insulin-like growth factor I (IGF-I) and its binding proteins IGFBP-1 and IGFBP-3
Authors: J L Chicharro, A López-Calderon, J Hoyos, A I Martín-Velasco, G Villa, M A Villanúa, A Lucía
Journal: British Journal of Sports Medicine (2001)

Objectives —To determine whether consecutive bouts of intense endurance exercise over a three week period alters serum concentrations of insulin-like growth factor I (IGF-I) and/or its binding proteins. Methods —Seventeen professional cyclists (mean (SEM) V o 2 max , 74.7 (2.1) ml/kg/min; age, 27 (1) years) competing in a three week tour race were selected as subjects. Blood samples were collected at each of the following time points: t 0 (control, before the start of competition), t 1 (end of first week), and t 3 (end of third week). Serum levels of both total and free IGF-I and IGF binding proteins 1 and 3 (IGFBP-1 and IGFBP-3) were measured in each of the samples. Cortisol levels were measured in nine subjects. Results —A significant (p&lt;0.01) increase was found in total IGF-I and IGFBP-1 at both t 1 and t 3 compared with t o (IGF-I: 110.9 (17.7), 186.8 (12.0), 196.9 (14.7) ng/ml at t 0 , t 1 , and t 3 respectively; IGFBP-1: 54.6 (6.6), 80.6 (8.0), and 89.2 (7.9) ng/ml at t 0 , t 1 , and t 3 respectively). A significant (p&lt;0.01) decrease was noted in free IGF-I at t 3 compared with both t o and t 1 (t 0 : 0.9 (0.1) ng/ml; t 1 : 0.9 (0.1) ng/ml; t 3 : 0.7 (0.1) ng/ml); in contrast, IGFBP-3 levels remained stable throughout the race. Conclusions —It would appear that the increase in circulating levels of both IGF-I and its binding protein IGFBP-1 is a short term (one week) endocrine adaptation to endurance exercise. After three weeks of training, total IGF-I and IGFBP-1 remained stable, whereas free IGF-I fell below starting levels.
Fetal-Derived Trophoblast Use the Apoptotic Cytokine Tumor Necrosis Factor-α–Related Apoptosis-Inducing Ligand to Induce Smooth Muscle Cell Death
Authors: Rosemary J. Keogh, Lynda K. Harris, Abigail Freeman, Philip N. Baker, John D. Aplin, Guy StJ. Whitley, Judith E. Cartwright
Journal: Circulation Research (2007)

Remodeling of the uterine spiral arteries during pregnancy transforms them from high to low resistance vessels that lack vasoconstrictive properties. This process is essential to meet the demand for increased blood flow imposed by the growing fetus. Loss of endothelial and smooth muscle cells (SMC) is evident in remodeled arteries but the mechanisms underlying this transformation remain unknown. This study investigated the hypothesis that fetal trophoblast invading from the placenta instigate remodeling by triggering cell death in vascular SMC. Specifically, a role for trophoblast-derived death inducing cytokine tumor necrosis factor-α–related apoptosis-inducing ligand (TRAIL) was investigated. Expression of the activating TRAIL receptors R1 and R2 was detected by flow cytometry on human aortic SMC and by immunohistochemistry on spiral artery SMC. Recombinant human TRAIL induced human aortic SMC apoptosis, which was inhibited by antibodies against TRAIL-R1 or -R2. Perfusion of denuded spiral artery segments with recombinant human TRAIL also induced SMC apoptosis. Trophoblasts isolated from first trimester placenta expressed membrane-associated TRAIL and induced apoptosis of human aortic SMC; apoptosis was significantly inhibited by a recombinant human TRAIL-R1:Fc construct. Trophoblast within the first trimester placental bed also expressed TRAIL. These data show that: 1) TRAIL causes SMC death; 2) trophoblast produce the apoptotic cytokine TRAIL; and 3) trophoblast induce SMC apoptosis via a TRAIL-dependent mechanism. We conclude that TRAIL produced by trophoblast causes apoptosis of SMC and thus may contribute to SMC loss during spiral artery remodeling in pregnancy.
Implication of Polycomb Members Bmi-1, Mel-18, and Hpc-2 in the Regulation of p16INK4a, p14ARF, h-TERT, and c-Myc Expression in Primary Breast Carcinomas
Authors: Javier Silva, José M. García, Cristina Peña, Vanesa García, Gemma Domínguez, Dolores Suárez, Francisca I. Camacho, Ruth Espinosa, Mariano Provencio, Pilar España, Félix Bonilla
Journal: Clinical Cancer Research (2006)

Abstract Purpose: Deregulation of mammalian Polycomb group (PcG) members may contribute to human carcinogenesis. p16INK4a and p14ARF tumor suppressors, human telomerase reverse transcriptase (h-TERT), and oncoprotein c-Myc have been implicated in the regulation of the cell cycle and proliferation mediated by PcG proteins, mainly Bmi-1, in mice and in cell culture experiments. Here, we examine whether these in vitro findings can be extrapolated to the in vivo situation. Experimental Design: We measure the expression of PcG members Bmi-1, Mel-18, and Hpc-2 and their potential targets by reverse transcription-PCR, immunostaining, and Western blotting in a series of 134 breast carcinomas and correlate the data with several clinical-pathologic variables of the tumors. Results: Expression of PcG genes was variably detected, but overexpression of Bmi-1 was the most frequent PcG alteration observed. In addition, statistical direct correlation in expression level of the three PcG members was detected. A correlation between c-Myc and Bmi-1 expression levels was observed; however, there was no correlation between expression of Bmi-1 and p16INK4a, p14ARF, or h-TERT. However, expression of the other PcG members Mel-18 and Hpc-2 correlated with the cell cycle regulators. Moreover, PcG mRNA–altered expression correlated significantly with certain clinical-pathologic variables associated with poor prognosis. Conclusions: Our data suggest that the oncogenic role of Bmi-1 in human primary breast carcinomas is not determined by its capacity to inhibit INK4a/ARF proteins or to induce telomerase activity.
CONNECTIVE TISSUE SYNTHESIS BY SCLERODERMA SKIN FIBROBLASTS IN CELL CULTURE
Authors: E. Carwile Leroy
Journal: The Journal of Experimental Medicine (1972)

Skin fibroblasts from subjects with scleroderma and control subjects were grown in tissue culture to compare the characteristics of connective tissue metabolism. A striking increase in soluble collagen (media hydroxyproline) was observed in eight of nine scleroderma cultures when they were compared with identically handled control cultures matched for the age and sex of the donor and the anatomic site of the donor skin. Glycoprotein content as estimated by hexosamine and sialic acid was also significantly increased in the scleroderma cultures. Estimations of protein-polysaccharide content by uronic acid determinations were low in all cultures and not significantly increased in scleroderma cultures. This report demonstrates the feasibility of using fibroblast cell cultures to study chronic rheumatic and connective tissue disorders. The initial results suggest a net increase in collagen and glycoprotein synthesis in scleroderma fibroblast cultures. The implications of an abnormality of connective tissue metabolism by skin fibroblasts propagated in vitro in the acquired disorder scleroderma are discussed.
Decreased glycolipid antigen expression in lymphoma cell variants escaping from anti-glycolipid serotherapy.
Authors: W W Young, Y Tamura, H S Johnson, D A Miller
Journal: The Journal of Experimental Medicine (1983)

Mice challenged with L5178Y lymphoma cells expression high levels of the glycolipid asialo GM2 (gangliotriosylceramide) were protected from tumor growth by passive administration of a monoclonal antibody specific for the glycolipid; in a few antibody-treated mice, ascites cells eventually proliferated which contained a reduced chemical quantity of the glycolipid antigen (3). We now report that the cells emerging from antibody-treated mice had abnormal marker chromosomes identical to those in the cells used for challenge, indicating that the emergent cells were progeny of the challenge inoculum. Flow cytometric analysis revealed that asialo GM2 was undetectable on the surface of greater than 95% of the tumor cells from antibody-treated mice, whereas surface display of H-2 determinants was unchanged from that of the cells used for challenge. Tumor cells arising in challenged but untreated mice consisted of a mixture of asialo GM2-positive and -negative cells, indicating the presence of selective pressures in these mice as well. None of the cells taken from tumor bearing mice differed significantly from the challenge cells in their susceptibility to natural killer cell attack, suggesting that resistance to natural killer cell lysis was not responsible for the proliferation of these cells in vivo. When cells derived from an antibody-treated mouse were used to challenge mice, serotherapy with anti-asialo GM2 had no effect on mouse survival. These results suggest that serotherapy may complement a host anti-tumor response, from which only asialo GM2 deficient cells can escape.
HLA Class I Antigen Down-Regulation in Primary Ovary Carcinoma Lesions: Association with Disease Stage
Authors: Marco Vitale, Giuseppe Pelusi, Beatrice Taroni, Giuliana Gobbi, Cristina Micheloni, Rita Rezzani, Francesco Donato, Xinhui Wang, Soldano Ferrone
Journal: Clinical Cancer Research (2005)

Abstract Purpose: To investigate TAP1, TAP2, and HLA class I antigen expression in primary ovarian carcinoma lesions and to assess the clinical significance of defects in the expression of these molecules. Experimental Design: Fifty-one formalin-fixed, paraffin-embedded primary ovarian carcinoma lesions were stained with affinity-purified rabbit anti-TAP1 and anti-TAP2 antibodies and with anti-HLA class I heavy chain monoclonal antibody (mAb) HC-10 using the immunoperoxidase reaction. The results of immunohistochemical staining were correlated with the histopathologic characteristics of the lesions and with patients' survival. Results: Ovarian surface epithelium, thecal cells of follicles, and stromal cells were stained by anti-TAP1, anti-TAP2, and anti-HLA class I antigen xenoantibodies with a homogeneous pattern. In contrast, no staining of lutheinic cells by these antibodies was detected. Forty-one and 32 out of 51 primary ovarian carcinoma lesions were stained by anti-TAP1 and anti-TAP2 xenoantibodies and by anti-HLA class I antigen mAb HC-10, respectively. The staining patterns by anti-TAP1 and anti-TAP2 xenoantibodies were completely concordant, but did not correlate with that by anti-HLA class I heavy chain mAb HC-10. TAP1 and TAP2 expression was associated neither with the histopathologic characteristics of the lesions nor with clinical variables. On the other hand, HLA class I antigen down-regulation was associated with disease stage: the odds ratio of stage III for HLA class I antigen negative patients was 7.6 (95% confidence interval, 1.9-30.5; P= 0.007), whereas for TAP negative patients was 5.1 (95% confidence interval, 0.9-28.4; P = 0.07). Follow up was available for 39 out of the 51 patients. Multivariate analysis showed that both grading and staging were associated with a higher risk of death, whereas TAP and HLA class I antigen phenotypes were not. Conclusions: The lack of association between TAP and HLA class I antigen expression is compatible with the possibility that multiple mechanisms underlie HLA class I antigen down-regulation in primary ovarian carcinoma lesions. The potential role of immunologic events in the clinical course of ovarian carcinoma suggests that the association between HLA class I antigen down-regulation and disease progression may reflect the escape of tumor cells from immune recognition and destruction.
Wheat Sensitization and Work-related Symptoms in the Baking Industry Are Preventable
Authors: REMKO HOUBA, DICK HEEDERIK, GERT DOEKES
Journal: American Journal of Respiratory and Critical Care Medicine (1998)

A cross-sectional study was conducted among 393 workers from 21 bakeries to study the relationship between wheat allergen exposure and wheat sensitization and work-related allergic symptoms. Exposure to wheat allergens was characterized by a recently developed and validated immunoassay. Specific IgE antibodies against wheat flour and common allergens were measured by immunoassays, and work-related allergic symptoms were registered by questionnaire. A strong and positive association was found between wheat flour allergen exposure and wheat flour sensitization. This relationship was steepest and strongest in atopics. Prevalence ratios for high and medium wheat allergen exposure were 5.2 (95% confidence interval [CI], 1.6-16.2), and 2.7 (0.5-14.5) for atopic workers, and 2.5 (0.8-7.5) and 1.4 (0. 3-6.4) for nonatopics, compared with workers with low wheat allergen exposure. In sensitized bakers those with an elevated allergen exposure had more often work-related symptoms, with prevalence ratios for high and medium wheat allergen exposure of 3.5 (CI 1.6-7. 5) and 2.6 (CI 0.9-7.8), respectively, compared with workers with low wheat allergen exposure. The existence of exposure-sensitization gradients suggests that work-related sensitization risk will be negligible when exposure levels will be reduced to average exposure concentration of 0.2 microgram/m3 wheat allergen or approximately 0.5 mg/m3 inhalable dust during a work shift.
Biologically Targeted Therapies Plus Chemotherapy Plus Radiotherapy in Stage III Non–Small-Cell Lung Cancer: A Case of the Icarus Syndrome?
Authors: David Raben, Paul A. Bunn
Journal: Journal of Clinical Oncology (2012)

The myth of Daedalus and Icarus has been around for over two thousand years, but it still offers a timely metaphor for many modern misadventures. The basic plotline is as follows: ambitious pioneers couple optimism and audacity with unfettered access to new technology or other innovations and launch themselves into a daring, dizzying adventure. Tragically, the story melts into a morality tale when Icarus flies too close to the sun, then crashes in spectacular fashion. The article 1 that accompanies this editorial describes a clinical trial with many of the hallmarks of the Icarus syndrome: the soaring attempt by Socinski et al 1 to conquer stage III non–small-cell lung cancer (NSCLC) with a bold phase I/II trial in which patients with stage NSCLC were treated with a combination of induction bevacizumab (15 mg/kg) and carboplatin-paclitaxel, followed by concurrent bevacizumab alone (cohort 1 at 10 mg/kg) or with erlotinib (100, 150 mg/kg for cohorts 2 and 3, respectively), with radiation (74 Gy) and weekly carboplatin-paclitaxel. This was followed with an attempt at consolidative erlotinib and bevacizumab for six cycles in a searing assault on this terrible disease. The tantalizing promise of breakthrough results from their uber-aggressive approach failed to materialize, leaving in its wake worrisome adverse effects that prevented the administration of all intended therapy without meaningful clinical gains and an underwhelming overall survival of 18.4 months. No analogy is perfect, and oncologists who treat lung cancer
Prioritizing Clinical Preventive Services: A Review and Framework with Implications for Community Preventive Services
Authors: Michael V. Maciosek, Ashley B. Coffield, Nichol M. Edwards, Thomas J. Flottemesch, Leif I. Solberg
Journal: Annual Review of Public Health (2009)

Setting priorities on the basis of factors such as health impact and economic value is the key first step to ensure that the most important services receive the most attention. Few prioritization efforts have been published that produce either rankings or information that can guide decision making. We propose a framework to help decision makers and clinicians balance short-term demands against long-term objectives. This framework provides guidance for decisions about scope, prioritization criteria, evidence review methods, evaluation of criteria fit, and presentation of results. The framework is the result of our experience setting priorities among clinical preventive services. It has not been tested in prioritizing community interventions and other health care services but should provide a useful starting point for designing priority-setting efforts in those areas.
Starting at the Beginning: New Perspectives on the Biology of Mucosal T Cells
Authors: Hilde Cheroutre
Journal: Annual Review of Immunology (2004)

The gastrointestinal tract is the central organ for uptake of fluids and nutrients, and at the same time it forms the main protective barrier between the sterile environment of the body and the outside world. In mammals, the intestine has further evolved to harbor a vast load of commensal bacteria that have important functions for the host. Discrimination by the host defense system of nonself from self can prevent invasion of pathogens, but equivalent responses to dietary or colonizing bacteria can lead to devastating consequences for the organism. This dilemma imposed by the gut environment has probably contributed significantly to the evolutionary drive that has led to sophisticated mechanisms and diversification of the immune system to allow for protection while maintaining the integrity of the mucosal barrier. The immense expansion and specialization of the immune system is particularly mirrored in the phylogeny, ontogeny, organization, and regulation of the adaptive intraepithelial lymphocytes, or IEL, which are key players in the unique intestinal defense mechanisms that have evolved in mammals.