tbuckley/cabot-search huggingface dataset:
Association Between Emphysema-like Lung on Cardiac Computed Tomography and Mortality in Persons Without Airflow Obstruction
Authors: Elizabeth C. Oelsner, Eric A. Hoffman, Aaron R. Folsom, J. Jeffrey Carr, Paul L. Enright, Steven M. Kawut, Richard Kronmal, David Lederer, Joao A.C. Lima, Gina S. Lovasi, Steven Shea, R. Graham Barr
Journal: Annals of Internal Medicine (2014)

Low lung function is known to predict mortality in the general population, but the prognostic significance of emphysema on computed tomography (CT) in persons without chronic obstructive pulmonary disease (COPD) is uncertain.To determine whether greater emphysema-like lung on CT is associated with all-cause mortality among persons in the general population without airflow obstruction or COPD.Prospective cohort study.Population-based, multiethnic sample from 6 U.S. communities.2965 participants aged 45 to 84 years without airflow obstruction on spirometry.Emphysema-like lung was defined as the number of lung voxels with attenuation less than -950 Hounsfield units on cardiac CT and was adjusted for the number of total imaged lung voxels.Among 2965 participants, 50.9% of whom had never smoked, there were 186 deaths over a median of 6.2 years. Greater emphysema-like lung was independently associated with increased mortality (adjusted hazard ratio per one-half interquartile range, 1.14 [95% CI, 1.04 to 1.24]; P=0.004) after adjustment for potential confounders, including cardiovascular risk factors and FEV1. Generalized additive models supported a linear association between emphysema-like lung and mortality without evidence for a threshold. The association was of greatest magnitude among smokers, although multiplicative interaction terms did not support effect modification by smoking status.Cardiac CT scans did not include lung apices. The number of deaths was limited among subgroup analyses.Emphysema-like lung on CT was associated with all-cause mortality among persons without airflow obstruction or COPD in a general population sample, particularly among smokers. Recognition of the independent prognostic significance of emphysema on CT among patients without COPD on spirometry is warranted.National Heart, Lung, and Blood Institute.
A Novel Set of DNA Methylation Markers in Urine Sediments for Sensitive/Specific Detection of Bladder Cancer
Authors: Jian Yu, Tongyu Zhu, Zhirou Wang, Hongyu Zhang, Ziliang Qian, Huili Xu, Baomei Gao, Wei Wang, Lianping Gu, Jun Meng, Jina Wang, Xu Feng, Yixue Li, Xuebiao Yao, Jingde Zhu
Journal: Clinical Cancer Research (2007)

Abstract Purpose: This study aims to provide a better set of DNA methylation markers in urine sediments for sensitive and specific detection of bladder cancer. Experimental Design: Fifty-nine tumor-associated genes were profiled in three bladder cancer cell lines, a small cohort of cancer biopsies and urine sediments by methylation-specific PCR. Twenty-one candidate genes were then profiled in urine sediments from 132 bladder cancer patients (8 cases for stage 0a; 68 cases for stage I; 50 cases for stage II; 4 cases for stages III; and 2 cases for stage IV), 23 age-matched patients with noncancerous urinary lesions, 6 neurologic diseases, and 7 healthy volunteers. Results: Despite six incidences of four genes reported in 3 of 23 noncancerous urinary lesion patients analyzed, cancer-specific hypermethylation in urine sediments were reported for 15 genes (P &amp;lt; 0.05). Methylation assessment of an 11-gene set (SALL3, CFTR, ABCC6, HPR1, RASSF1A, MT1A, RUNX3, ITGA4, BCL2, ALX4, MYOD1, DRM, CDH13, BMP3B, CCNA1, RPRM, MINT1, and BRCA1) confirmed the existing diagnosis of 121 among 132 bladder cancer cases (sensitivity, 91.7%) with 87% accuracy. Significantly, more than 75% of stage 0a and 88% of stage I disease were detected, indicating its value in the early diagnosis of bladder cancer. Interestingly, the cluster of reported methylation markers used in the U.S. bladder cancers is distinctly different from that identified in this study, suggesting a possible epigenetic disparity between the American and Chinese cases. Conclusions: Methylation profiling of an 11-gene set in urine sediments provides a sensitive and specific detection of bladder cancer.
Repression of microRNA-130b by thyroid hormone enhances cell motility
Authors: Yang-Hsiang Lin, Meng-Han Wu, Chia-Jung Liao, Ya-Hui Huang, Hsiang-Cheng Chi, Sheng-Ming Wu, Cheng-Yi Chen, Yi-Hsin Tseng, Chung-Ying Tsai, I-Hsiao Chung, Ming-Ming Tsai, Ching-Ying Chen, Tina P. Lin, Yung-Hsin Yeh, Wei-Jan Chen, Kwang-Huei Lin
Journal: Journal of Hepatology (2015)
Abstract 1266: TNF-alpha mediated down-regulation of Na+/H+ exchanger 1 (NHE1) in breast cancer MCF7 cells and its relevance to apoptosis
Authors: Sui Huay Chua, Marie V. Clement
Journal: Cancer Research (2010)

Abstract Intracellular alkalinization is a hallmark of cancer cells shown to confer resistance against caspase mediated apoptosis. Na+/H+ exchanger 1 (NHE1), an ion exchanger important in the maintenance of intracellular pH and cell volume homeostasis had been implicated in this intracellular alkalinization. Increased NHE1 protein level and activity has been found in many cancer cells types where increase in intracellular pH by constitutively active NHE1 confers resistance to apoptosis in these cells. Silencing of NHE1 protein in cancer cells results in reduced cell growth and increased in sensitivity to death triggers. TNF-α can induce H2O2 production in cells to mediate apoptosis with characteristic cell shrinkage. H2O2 had recently been shown to downregulate NHE1 expression and increase cells’ sensitivity to apoptosis. This study was undertaken to study the role of caspases and H2O2 in the regulation of NHE1 protein and gene expression by TNF-α. Results showed that TNF-α had both cytostatic and cytotoxic effects on MCF-7 cells with concurrent decrease in intracellular pH and NHE1 activity. NHE1 was found to be downregulated both at the protein and mRNA level following TNF-α treatment. Gelshift assay showed that transcription factors binding to the promoter of NHE1 could be blocked by pre-incubation with H2O2, suggesting that transcription of NHE1 could be redox-regulated. Indeed, we also show by using a luciferase reporter assay that NHE1 promoter is down-regulated in presence of H2O2. Various caspases were activated in TNF-α treated cells and the inhibition of caspases prevented the downregulation of NHE1. ROS was elevated in MCF-7 within 2 hours of treatment. Incubation of cells with catalase increased their survival in response to TNF-α, thus implicating H2O2 as a mediator of TNF-α induced cell death. Overexpression of catalase in MCF-7 reduced the downregulation of NHE1 by TNF-α. Our results suggest by TNF-α mediate cell death through decreasing NHE1 activity and down-regulating NHE1 expression in a ROS mediated manner. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1266.
I Am, as Usual, Fuming-Reply
Authors: Kevin Grumbach
Journal: JAMA (1995)

In Reply.  —Dr Morgan takes issue with some of the clinical vignettes in one of the recent installments in our series Health Care Policy: A Clinical Approach. These vignettes, used to attempt to illustrate basic principles in the series, are usually drawn from our own experiences as clinicians or the experiences of colleagues and patients. The first of the vignettes mentioned by Morgan illustrates the importance of a primary caregiver to coordinate referral services. We did not intend to imply that the primary care clinician in this scenario (a nurse practitioner) necessarily completely supplants the oncologist or gastroenterologist, but rather that she helps to integrate care (eg, by communicating with the different specialists involved in caring for this patient). This coordinating function of the primary care provider is particularly important to protect against fragmentation of care when, for example, patients have multiple medical problems and do, in fact, require the
Aggregated neutrophil extracellular traps limit inflammation by degrading cytokines and chemokines
Authors: Christine Schauer, Christina Janko, Luis E Munoz, Yi Zhao, Deborah Kienhöfer, Benjamin Frey, Michael Lell, Bernhard Manger, Jürgen Rech, Elisabeth Naschberger, Rikard Holmdahl, Veit Krenn, Thomas Harrer, Ivica Jeremic, Rostyslav Bilyy, Georg Schett, Markus Hoffmann, Martin Herrmann
Journal: Nature Medicine (2014)
Brain shrinkage in chronic alcoholics: a pathological study.
Authors: C G Harper, J J Kril, R L Holloway
Journal: BMJ (1985)

A quantitative neuropathological necropsy study of 22 control and 22 chronic alcoholic subjects showed a statistically significant loss of brain tissue in the chronic alcoholic group. The loss of tissue appeared to be from the white matter of the cerebral hemispheres rather than the cerebral cortex. This may reflect a primary alteration in the composition or structure of the white matter or it may be secondary to loss of nerve cells from the cortex with subsequent degeneration of the axons in the white matter. Further morphometric analyses including cortical neuronal counts will be necessary to clarify this issue.
CHARACTERISTICS OF IMMUNOLOGICAL MEMORY IN MICE
Authors: S. J. Black, C. J. Inchley
Journal: The Journal of Experimental Medicine (1974)

The kinetics of the generation of primed IgM and IgG antibody-forming cell precursors, and of helper T-cell populations, were analyzed in mice whose primary responses to high and low doses of SRBC were arrested at intervals by the immunosuppressive agents cyclophosphamide monohydrate and specific antibody. The extent to which immunological memory was established in these animals before blockade of the primary response was assessed by the hemolytic plaque assay following challenge 12 wk after priming. The presence of IgG B-memory cells and T-memory cells in suppressed mice was further investigated by the transfer into these animals of syngeneic SRBC-stimulated thymocytes or anti-θ-treated spleen cells. It was found that the progenitors of secondary IgM-synthesizing cells were primed almost immediately after injection of antigen, and that early blockade of the primary response resulted in a raised IgM response after challenge. On the other hand, priming for a secondary IgG response took at least 4 days, and was dose-dependent, although helper T populations for a secondary IgG response appeared 3 days after antigen injection. It appeared that both IgM and IgG memory cells may be considered as Y cells in terms of the X-Y-Z scheme of lymphocyte activation, but that the two populations are generated at different times after exposure to antigen. The size of either Y-cell population at any given time is dependent upon the amount of antigen available to provoke differentiation to antibody-forming Z cells, and the IgM Y-cell population in particular is likely to be depleted during the course of a normal 1° response. When IgM Y cells were maintained for long periods as a result of immunosuppression, their secondary antibody response was independent of the primed T cells necessary for a secondary IgG response.
STRANGULATED FEMORAL HERNIA IN A WOMAN, AGED 107 YEARS
Authors: H. W. Vickers
Journal: JAMA (1923)

This case is of interest solely because of the advanced age of the patient. Mrs. D. F., a woman, aged 107, referred to me by Dr. Edgar Swift, Jordanville, N. Y., June 19, 1922, was suffering from a strangulated femoral hernia that could not be reduced. The patient, born May 4, 1815, in the town of Stark, Herkimer County, N. Y., came from a healthy, long-lived race. Her father died at the age of 97; her mother, at the age of 76; a brother, at 95, and her husband at 80. Recently a nephew died at 87. She was married at the age of 19, and had borne six children, two of whom were living, one being over 83 years. She had always been well, a frugal eater, very calm and mild in disposition, contented and a great worker. The patient stated that until four years ago she had always
Bmi-1 is induced by the Epstein-Barr virus oncogene LMP1 and regulates the expression of viral target genes in Hodgkin lymphoma cells
Authors: Amanda Dutton, Ciaran B. Woodman, Marilyn B. Chukwuma, James I. K. Last, Wenbin Wei, Martina Vockerodt, Karl R. N. Baumforth, Joanne R. Flavell, Martin Rowe, A. Malcolm R. Taylor, Lawrence S. Young, Paul G. Murray
Journal: Blood (2006)
Polycyclic Aromatic Hydrocarbons–Aromatic DNA Adducts in Cord Blood and Behavior Scores in New York City Children
Authors: Frederica P. Perera, Shuang Wang, Julia Vishnevetsky, Bingzhi Zhang, Kathleen J. Cole, Deliang Tang, Virginia Rauh, David H. Phillips
Journal: Environmental Health Perspectives (2011)

Background: Airborne polycyclic aromatic hydrocarbons (PAH) are widespread urban pollutants that can bind to DNA to form PAH–DNA adducts. Prenatal PAH exposure measured by personal monitoring has been linked to cognitive deficits in childhood in a prospective study conducted by the Columbia Center for Children's Environmental Health.Objectives: We measured PAH–DNA and other bulky aromatic adducts in umbilical cord white blood cells using the 32P-postlabeling assay to determine the association between this molecular dosimeter and behavioral/attention problems in childhood.Methods: Children born to nonsmoking African-American and Dominican women residing in New York City (NYC) were followed from in utero to 7–8 years of age. At two time points before 8 years of age (mean ages, 4.8 years and 7 years), child behavior was assessed using the Child Behavior Checklist (CBCL). To estimate and test the association between adducts and behavioral outcomes, both CBCL continuous raw scores and dichotomized T-scores were analyzed.Results: Higher cord adducts were associated with higher symptom scores of Anxious/Depressed at 4.8 years and Attention Problems at 4.8 and 7 years, and with Diagnostic and Statistical Manual of Mental Disorders, 4th edition–oriented Anxiety Problems at 4.8 years.Conclusions: These results suggest that PAH exposure, measured by DNA adducts, may adversely affect child behavior, potentially affecting school performance.
"Airplane" Splint for Forearm Fractures in Children
Authors: J. Lorin Mason
Journal: JAMA (1965)

POSTREDUCTION swelling and Volkmann's ischemic contracture are the most common and most feared complications of fractures of the forearm in children. The following method of assuring forearm elevation is proposed in an attempt to reduce the chances of inadequate venous drainage, regardless of whether the patient is hospitalized or is treated as an outpatient.  No originality is claimed for this method; I feel sure that other physicians have used this method. However, a review of the literature did not reveal publication of this procedure. There are many methods of assuring elevation, but this method seems to be the most foolproof way of assuring adequate elevation by mechanical means.  This splint affords some hindrance to getting about, and will help in keeping the small child inactive during the danger period of the first 24 to 48 hours immediately after the fracture. The only comfortable position is to have the splint resting
Part 2: The Cluster Headache
Authors: Roger C. Duvoisin
Journal: JAMA (1972)

Within the migraine family there is a very distinctive variety of headache. The symptoms are unilateral, abrupt in onset, brief in duration, and appear consistently on the same side. Attacks recur often, usually daily, with remarkable regularity, for a period of one or two months and then subside to return only after an interval of months or years. Because of this distinctive temporal pattern, the descriptive term "cluster headache" suggested by Kunkle et al<sup>1</sup>a number of years ago has gained general recognition and largely displaced previous designations such as histamine cephalgia, ciliary neuralgia, and periodic migrainous cephalgia. <h3>Symptoms</h3> The typical patient with cluster headache seeks medical aid because of a unilateral headache recurring frequently, perhaps daily, which is not relieved by the usual analgesics. The headache begins suddenly and without warning, with a pulling, tugging, or pressing sensation behind one eye. It progresses rapidly within minutes to a
Statement on malignant mesothelioma in the UK
Authors: M Robinson
Journal: Thorax (2002)

Tattersfield et al 1 and Walsh et al 2 offer important information about the possible adverse affects of corticosteroids on bone mineral density (BMD).Tattersfield and her colleagues reported no change in BMD with inhaled corticosteroids for mild asthma, while Walsh et al found a dose related increase in the incidence of fractures in those taking oral corticosteroids.We would like to report our study of BMD in patients with airways disease, which reinforces these findings and highlights men as being particularly at risk.We prospectively studied 100 consecutive outpatients (44 men) with steroid responsive airways disease.The formulation and cumulative dose of corticosteroid was recorded in each individual, together with all prescribed prophylaxis for osteoporosis.Bone mineral density was measured in the non-dominant forearm.We found no relationship between inhaled corticosteroid dose and BMD.Mean BMD was significantly reduced in those on oral as opposed to inhaled steroids.In men the mean Z scores for those on inhaled and oral corticosteroids were 0.1 and -0.6, respectively (p=0.07), while women had mean Z scores of 0.5 and -0.3 for inhaled and oral corticosteroids, respectively (p=0.016).Our patient numbers were insufficient to confirm a dose response.The surprising result was that men were more likely to meet the WHO criteria for osteoporosis than women (25% v 12.5%).This result is explained at least in part by the use of prophylaxis which was prescribed to 21 women but to only two men.Of those on regular oral steroids, only 5.5% of men received prophylaxis compared with 62.5% of women.Similar results have been reported in other chronic diseases, with a greater reduction in BMD being reported in men with cystic fibrosis. 3 Unfortunately it appears to have been assumed that men are protected from osteoporosis by virtue of their gender.When chronic disease is treated with oral corticosteroids, both men and women are equally at risk of osteoporosis and all should be considered for prophylaxis.
HIV-1 Viremia Prevents the Establishment of Interleukin 2–producing HIV-specific Memory CD4+ T Cells Endowed with Proliferative Capacity
Authors: Souheil-Antoine Younes, Bader Yassine-Diab, Alain R. Dumont, Mohamed-Rachid Boulassel, Zvi Grossman, Jean-Pierre Routy, Rafick-Pierre Sékaly
Journal: The Journal of Experimental Medicine (2003)

CD4+ T cell responses are associated with disease control in chronic viral infections. We analyzed human immunodeficiency virus (HIV)-specific responses in ten aviremic and eight viremic patients treated during primary HIV-1 infection and for up to 6 yr thereafter. Using a highly sensitive 5-(and-6)-carboxyfluorescein diacetate-succinimidyl ester–based proliferation assay, we observed that proliferative Gag and Nef peptide-specific CD4+ T cell responses were 30-fold higher in the aviremic patients. Two subsets of HIV-specific memory CD4+ T cells were identified in aviremic patients, CD45RA− CCR7+ central memory cells (Tcm) producing exclusively interleukin (IL)-2, and CD45RA− CCR7− effector memory cells (Tem) that produced both IL-2 and interferon (IFN)-γ. In contrast, in viremic, therapy-failing patients, we found significant frequencies of Tem that unexpectedly produced exclusively IFN-γ. Longitudinal analysis of HIV epitope–specific CD4+ T cells revealed that only cells that had the capacity to produce IL-2 persisted as long-term memory cells. In viremic patients the presence of IFN-γ–producing cells was restricted to periods of elevated viremia. These findings suggest that long-term CD4+ T cell memory depends on IL-2–producing CD4+ T cells and that IFN-γ only–producing cells are short lived. Our data favor a model whereby competent HIV-specific Tcm continuously arise in small numbers but under persistent antigenemia are rapidly induced to differentiate into IFN-γ only–producing cells that lack self-renewal capacity.
Decreased cyclin B1 expression contributes to G2 delay in human brain tumor cells after treatment with camptothecin
Authors: Anna J. Janss, Amit Maity, Cheng-Bi Tang, Ruth J. Muschel, W. Gillies McKenna, Leslie Sutton, Peter C. Phillips
Journal: Neuro-Oncology (2001)

DNA damage produces delayed mitosis (G2/M delay) in proliferating cells, and shortening the delay sensitizes human malignant glioma and medulloblastoma cells to cytotoxic chemotherapy. Although activation of the cyclin-dependent kinase CDC2 mediates G2/M transition in all tumor cells studied to date, regulation of CDC2 varies between tumor types. Persistent hyperphosphorylation of kinase and reduced cyclin expression have been implicated as mediators of treatment-induced G2 delay in different tumor models. To evaluate regulation of G2/M transition in human brain tumors, we studied the expression and/or activity of CDC2 kinase and cyclins A and B1 in U-251 MG and DAOY medulloblastoma cells after their treatment with camptothecin (CPT). Synchronized cells were treated during S phase, then harvested at predetermined intervals for evaluation of cell cycle kinetics, kinase activity mRNA, and protein expression. CPT produced G2 delay associated with decreased CDC2 kinase activity and cyclin B1 expression. Kinase activity was associated with CDC2 bound to cyclin B1, not cyclin A, in both cell lines. Cyclin A mRNA and protein expression were reduced after CPT treatment; however, decreased protein expression was short lived and moderate in the glioma and primitive neuroectodermal tumor/medulloblastoma cells, respectively. We conclude that G2 delay is a common response of brain tumor cells to chemotherapy with topoisomerase I inhibitors and that a mechanism of this delay may be reduced expression of cyclin B1.