tbuckley/cabot-search huggingface dataset:
Pulmonary function tests and high resolution computed tomography of the lungs in patients with rheumatoid arthritis
Authors: B. Cortet, T. Perez, N. Roux, R.-M. Flipo, B. Duquesnoy, B. Delcambre, M. Remy-Jardin
Journal: Annals of the Rheumatic Diseases (1997)

<h3>OBJECTIVE</h3> To compare the results of pulmonary function tests (PFTs) and high resolution computed tomography (HRCT) of the lungs in rheumatoid arthritis (RA) patients. <h3>METHODS</h3> Sixty eight patients (54 women, 14 men) fulfilling the revised criteria for RA were consecutively included in a transversal prospective study. Their mean age was 58.8 years (range: 35–82) and the mean duration of the disease was 12 years (range: 5–16). Rheumatoid factor was positive in 52 patients (76.5%). Fifty two patients (76.5%) were lifelong non-smokers. Detailed medical and drug histories were obtained. PFTs comprised spirometry and gas transfer measurements. Results for PFTs were expressed as percentage of predicted values for each individual adjusted for age, sex, and height. HRCT was undertaken with a Siemens Somatom Plus. <h3>RESULTS</h3> A significant decrease of FEV1/FVC, FEF25%, FEF50%, FEF75%, FEF25–75%, and TLCO was observed (p&lt;0.05) and 13.2% of the patients had a small airways involvement defined by a decrease of FEF25–75% below 1.64 SD. The most frequent HRCT findings were: bronchiectasis (30.5%), pulmonary nodules (28%), and air trapping (25%). The patients with small airways involvement had a high frequency of recurrent bronchitis (75% <i>v</i> 34%, p=0.05) and bronchiectasis (71% <i>v</i> 23%, p=0.019). The patients with bronchiectasis were characterised by low values of FEV1, FVC, FEF25–75%, and TLCO (p&lt;0.01), a high prevalence of small airways involvement (29% <i>v</i> 5%, p=0.019), and a low prevalence of HLA DQA1 *0501 allele (14% <i>v</i> 33%, p&lt;0.05). <h3>CONCLUSION</h3> This study suggests a significant association between small airways involvement on PFTs and bronchiectasis on HRCT in unselected RA patients.
Distribution and clonal relationship of cell surface virulence genes among Streptococcus pneumoniae isolates in Japan
Authors: S. Imai, Y. Ito, T. Ishida, T. Hirai, I. Ito, K. Yoshimura, K. Maekawa, S. Takakura, A. Niimi, Y. Iinuma, S. Ichiyama, M. Mishima
Journal: Clinical Microbiology and Infection (2010)
MEMBRANE ANTIGENS SPECIFIC FOR HUMAN LYMPHOID CELLS IN THE DIVIDING PHASE
Authors: D. B. Thomas, B. Phillips
Journal: The Journal of Experimental Medicine (1973)

Heteroantisera were raised in rabbits against human thymocytes or Burkitt's lymphoma EBI cells. After suitable absorption, the sera were specific for thymocytes and T lymphoblasts, or B lymphoblasts and several lymphoblastoid cell lines. The specificity of the antisera was confirmed by preparing purified populations of T or B lymphocytes on immunoabsorbent columns, followed by mitogenic stimulation with phytohemagglutinin. The antisera did not react with normal resting lymphocytes.
Mutational and Biological Analysis of α-Actinin-4 in Focal Segmental Glomerulosclerosis
Authors: Astrid Weins, Peter Kenlan, Stephanie Herbert, Tu C. Le, Ivan Villegas, Bernard S. Kaplan, Gerald B. Appel, Martin R. Pollak
Journal: Journal of the American Society of Nephrology (2005)

Mutations in the alpha-actinin-4 gene (ACTN4) cause an autosomal dominant form of focal segmental glomerulosclerosis (FSGS). A mutational analysis was performed of ACTN4 in DNA from probands with a family history of FSGS as well as in individuals with nonfamilial FSGS. The possible contribution of noncoding variation in ACTN4 to the development of FSGS also was assessed. Multiple nucleotide variants were identified in coding and noncoding sequence. The segregation of nonsynonymous coding sequence variants was examined in the relevant families. Only a small number of nucleotide changes that seemed likely to be causing (or contributing to) disease were identified. Sequence changes that predicted I149del, W59R, V801M, R348Q, R837Q, and R310Q changes were identified. For studying their biologic relevance and their potential roles in the pathogenesis of FSGS, these variants were expressed as GFP-fusion proteins in cultured podocytes. F-actin binding assays also were performed. Three of these variants (W59R, I149del, and V801M) showed clear cellular mislocalization in the form of aggregates adjacent to the nucleus. Two of these mislocalized variants (W59R and I149del) also showed an increased actin-binding activity. The I149del mutation segregated with disease; W59R was found to be a de novo mutation in the proband. A total of five ACTN4 mutations that are believed to be disease causing (three reported previously and two novel) as well as a number of variants with unclear contribution to disease now have been identified. The possibility that some of these other variants increase the susceptibility to FSGS cannot be excluded. ACTN4 mutations seem to account for approximately 4% of familial FSGS.
A Small N-Terminal 60-kD Fragment of gp600 (Megalin), the Major Autoantigen of Active Heymann Nephritis, Can Induce a Full-Blown Disease
Authors: ANDREW V. OLEINIKOV, BRADY J. FELIZ, SUDESH P. MAKKER
Journal: Journal of the American Society of Nephrology (2000)

Active Heymann nephritis of rat, an autoimmune glomerular disease, is an immunohistological, ultrastructural, and clinical model of human membranous glomerulonephritis. Both diseases in their full-blown form are characterized by (1) the formation of large, subepithelial glomerular immune deposits, which stain for IgG, C3, and membrane attack (C5b-9) components of complement and (2) the excretion of large amounts of protein in the urine (proteinuria). The target autoantigen of active Heymann nephritis is a large transmembrane renal glycoprotein with a molecular weight of approximately 600 kD, variously named gp600, gp330, LRP-2, or "megalin." This study was performed to identify the region in this enormously large glycoprotein that would produce full-blown active Heymann nephritis. A stable, small (60-kD) proteolytic fragment of gp600 was isolated and localized to the N-terminal end of the molecule using Western blot, sequencing, and amino acid analyses. Based on its primary structure, this fragment contains approximately 60 cysteine residues, the cross-linking of which to each other probably explains its stability. Immunization of rats with this fragment induced a full-blown disease that was comparable to the disease induced by a preparation containing the whole protein. These results indicate that this small fragment, retaining the natural disulfide bonds and probably its overall structure, contains those B and T cell epitopes that are sufficient to produce this organ-specific autoimmune disease.
TRANSCRIPTION FACTORS OF THE NFAT FAMILY:Regulation and Function
Authors: Anjana Rao, Chun Luo, Patrick G. Hogan
Journal: Annual Review of Immunology (1997)

▪ Abstract As targets for the immunosuppressive drugs cyclosporin A and FK506, transcription factors of the NFAT (nuclear factor of activated T cells) family have been the focus of much attention. NFAT proteins, which are expressed in most immune-system cells, play a pivotal role in the transcription of cytokine genes and other genes critical for the immune response. The activity of NFAT proteins is tightly regulated by the calcium/calmodulin-dependent phosphatase calcineurin, a primary target for inhibition by cyclosporin A and FK506. Calcineurin controls the translocation of NFAT proteins from the cytoplasm to the nucleus of activated cells by interacting with an N-terminal regulatory domain conserved in the NFAT family. The DNA-binding domains of NFAT proteins resemble those of Rel-family proteins, and Rel and NFAT proteins show some overlap in their ability to bind to certain regulatory elements in cytokine genes. NFAT is also notable for its ability to bind cooperatively with transcription factors of the AP-1 (Fos/Jun) family to composite NFAT:AP-1 sites, found in the regulatory regions of many genes that are inducibly transcribed by immune-system cells. This review discusses recent data on the diversity of the NFAT family of transcription factors, the regulation of NFAT proteins within cells, and the cooperation of NFAT proteins with other transcription factors to regulate the expression of inducible genes.
Relation of Postural Vasovagal Syncope to Splanchnic Hypervolemia in Adolescents
Authors: Julian M. Stewart, Kenneth J. McLeod, Sanjukta Sanyal, Gilbert Herzberg, Leslie D. Montgomery
Journal: Circulation (2004)

The mechanisms of simple faint remain elusive. We propose that postural fainting is related to excessive thoracic hypovolemia and splanchnic hypervolemia during orthostasis compared with healthy subjects.
Risk Factors for Venous Thromboembolism
Authors: Frederick A. Anderson, Frederick A. Spencer
Journal: Circulation (2003)

Until the 1990s, venous thromboembolism (VTE) was viewed primarily as a complication of hospitalization for major surgery (or associated with the late stage of terminal illness). However, recent trials in patients hospitalized with a wide variety of acute medical illnesses have demonstrated a risk of VTE in medical patients comparable with that seen after major general surgery. In addition, epidemiologic studies have shown that between one quarter and one half of all clinically recognized symptomatic VTEs occur in individuals who are neither hospitalized nor recovering from a major illness. This expanding understanding of the population at risk challenges physicians to carefully examine risk factors for VTE to identify high-risk patients who could benefit from prophylaxis. Factors sufficient by themselves to prompt physicians to consider VTE prophylaxis include major surgery, multiple trauma, hip fracture, or lower extremity paralysis because of spinal cord injury. Additional risk factors, such as previous VTE, increasing age, cardiac or respiratory failure, prolonged immobility, presence of central venous lines, estrogens, and a wide variety of inherited and acquired hematological conditions contribute to an increased risk for VTE. These predisposing factors are seldom sufficient by themselves to justify the use of prophylaxis. Nevertheless, individual risk factors, or combinations thereof, can have important implications for the type and duration of appropriate prophylaxis and should be carefully reviewed to assess the overall risk of VTE in each patient.
A case study of the reproducibility of transcriptional reporter cell-based RNAi screens in Drosophila
Authors: Ramanuj DasGupta, Kent Nybakken, Matthew Booker, Bernard Mathey-Prevot, Foster Gonsalves, Binita Changkakoty, Norbert Perrimon
Journal: Genome biology (2007)

Off-target effects have been demonstrated to be a major source of false-positives in RNA interference (RNAi) high-throughput screens. In this study, we re-assess the previously published transcriptional reporter-based whole-genome RNAi screens for the Wingless and Hedgehog signaling pathways using second generation double-stranded RNA libraries. Furthermore, we investigate other factors that may influence the outcome of such screens, including cell-type specificity, robustness of reporters, and assay normalization, which determine the efficacy of RNAi-knockdown of target genes.
A Novel, Short, and Simple Questionnaire to Measure Health-related Quality of Life in Patients with Chronic Obstructive Pulmonary Disease
Authors: TAKASHI HAJIRO, KOICHI NISHIMURA, PAUL W. JONES, MITSUHIRO TSUKINO, AKIHIKO IKEDA, HIROSHI KOYAMA, TAKATERU IZUMI
Journal: American Journal of Respiratory and Critical Care Medicine (1999)

A novel, short, and simple questionnaire, the Airways Questionnaire 20 (AQ20), has been developed to measure and quantify disturbances in the health-related quality of life (HRQoL) of patients with asthma or chronic obstructive pulmonary disease (COPD). The AQ20 has 20 items with yes/no responses, and should take 2 min to complete and score. The purpose of this study was to assess the discriminative properties and responsiveness of the AQ20 in patients with COPD. First, in a cross- sectional study, 165 patients with mild-to-severe COPD (mean age, 69 +/- 7 yr; FEV1, 40 +/- 16% of predicted) completed the AQ20, the St. George's Respiratory Questionnaire (SGRQ), the Chronic Respiratory Disease Questionnaire (CRQ), pulmonary function tests, a progressive cycle ergometer exercise test, and an assessment of their dyspnea and anxiety. The score distribution of the AQ20 was skewed toward the mild end of the scale, whereas the SGRQ and CRQ showed a normal distribution. The AQ20 showed a moderately strong correlation with the maximal oxygen uptake and the assessment of dyspnea (Spearman's correlation coefficients [rs] = -0.49, -0.60, respectively), but a weak correlation with the FEV1 (rs = -0.18). Moderate to strong correlations were also recognized between the AQ20 and SGRQ and CRQ (rs = -0.80, -0.72, respectively). Multiple regression analysis revealed that dyspnea and anxiety accounted for 43% of the variance in the AQ20, almost the same as in the SGRQ and CRQ. Second, longitudinal changes over time in the FEV1, AQ20, SGRQ, and CRQ were examined in 86 patients with newly detected COPD (mean age, 69 +/- 8 yr; FEV1, 45 +/- 19% of predicted). All three measures showed significant improvements in their scores over a 3-mo period after initiating medical intervention. The change in the AQ20 showed a moderate to strong correlation with each dimension of the SGRQ and CRQ (rs = 0.56, -0.52, respectively), but no significant correlation was noted with the FEV1. In conclusion, the AQ20 may have discriminative properties and responsiveness that are similar to more complex questionnaires such as the SGRQ and CRQ. Because it is short and can be quickly answered and scored, the AQ20 may be useful in studies with limited time for HRQoL assessments.
Thanking our peer reviewers
Authors: Alan Storey
Journal: Molecular Cancer (2013)

As 2013 commences I would like to take a moment to reflect and recognize the peer reviewers that made the previous year possible. Listed below are those people who reviewed for Molecular Cancer last year. All are generous individuals who donated their time to assessing and improving our authors’ submissions. Your combined efforts have been invaluable to the editorial staff in maintaining the continued success of the journal in the Open Access forum. The editors of Molecular Cancer would like to thank all the reviewers who contributed to the journal in Volume 11 (2012) by participating in the review process - taking time out of your busy schedules and even to volunteer - without your critical insights, hard work and support for the journal we wouldn’t be able to do what we do.
Pattern of rheumatoid arthritis in West Malaysia.
Authors: B H Toh, S Sengupta, A H Ang, J C White, K S Lau
Journal: Annals of the Rheumatic Diseases (1973)

Common diseases are subject to considerable variation in incidence and expression due to influence of geographical factors, and rheumatoid arthritis (RA) is an example of this.Greenwood (1969) indicated that RA in tropical Africa is more benign than in temperate climates.In West Malaysia the severity and incidence appear to be intermediate between that in tropical Africa and in the temperate zones.Environmental, ethnic, and social factors interact in determining the pattern.Furthermore, the condition occurs at equivalent incidence with other rheumatic disorders, particularly gout and auto- immune disease as systemic lupus erythematosus (SLE).This report is a study of RA in the three main ethnic groups in West Malaysia. Material and methodsThe 57 patients attended the Arthritis Clinic, University Hospital, Kuala Lumpur, during 1967-70 and satisfied American Rheumatism Association criteria of 'definite'.RA (Ropes, Bennett, Cobb, Jacox, and Jessar, 1959).A further 21 cases of 'probable' RA have been excluded. JointsIn the clinical assessment, the joints were examined according to the method of Beetham, Polky, Slocomb, and Weaver (1965).Laboratory investigations(1) Haematology (Dacie and Lewis, 1968).(2) Urine analysis.(3) Stool for ankylostomiasis.(4) Serum proteins, uric acid, and blood urea.(5) Serology: Waaler-Rose, latex-fixation for rheuma- toid factor (RF, Hyland), antistreptolysin-O titre (Difco), LE cell, and blood Kahn tests.The Waaler-Rose test was done according to the method of Dacie and Lewis (1968).The latex-fixation test with human gamma-globulin for RF was performed on a Controls Blood and serum samples were obtained from medical students and the inhabitants of various rural and semi- rural areas. ResultsTable I shows the number of patients with RA.Compared with other joint conditions, RA and gout provided the majority of patients.Data on rheumatic fever, and septic, tuberculous, and post-traumatic arthritis have been excluded.Out of 53 patients with SLE seen during the period of this study, 35 had joint symptoms (Table I , overleaf).Ofthe 57 patients with definite RA, 27 were Chinese, 17 Indians, and 13 Malays (Table II).Female prepon- derance was noted in all three ethnic groups, the overall ratio being 4-2 to 1.The age at onset is shown in Fig. 1.In most patients the illness started when they were between 26 and 65 years.At presentation they had been ill for periods from a few weeks to 21 years: 29 for up to 1 year, seventeen for 2 to 5 years, and eleven for more than 5 years.A history of morning stiffness was given in almost all instances.
Evidence of neurodegeneration in autism spectrum disorder
Authors: Janet K Kern, David A Geier, Lisa K Sykes, Mark R Geier
Journal: Translational Neurodegeneration (2013)

Autism spectrum disorder (ASD) is a neurological disorder in which a significant number of children experience a developmental regression characterized by a loss of previously-acquired skills and abilities. Loss of neurological function in ASD, as observed in affected children who have regressed, can be explained as neurodegeneration. Although there is research evidence of neurodegeneration or progressive encephalopathy in ASD, the issue of neurodegeneration in ASD is still under debate. Evidence of neurodegeneration in the brain in ASD includes: (1) neuronal cell loss, (2) activated microglia and astrocytes, (3) proinflammatory cytokines, (4) oxidative stress, and (5) elevated 8-oxo-guanosine levels. The evidence from this review suggests that neurodegeneration underlies the loss of neurological function in children with ASD who have experienced regression and loss of previously acquired skills and abilities, and that research into treatments to address the issue of neurodegeneration in ASD are warranted.
MicroRNA-155 is essential for TH2-mediated allergen-induced eosinophilic inflammation in the lung
Authors: Carina Malmhäll, Sahar Alawieh, You Lu, Margareta Sjöstrand, Apostolos Bossios, Maria Eldh, Madeleine Rådinger
Journal: Journal of Allergy and Clinical Immunology (2013)
Regression of Left Ventricular Hypertrophy
Authors: Arnold M. Katz
Journal: Circulation (1998)

nly a decade ago, end-stage heart failure was viewed as an irreversible condition for which therapy could offer only transient symptomatic relief.This led to a sense of hopelessness that resembled the prevailing attitude toward coronary occlusive disease 50 years ago, when atherosclerosis was thought to be an inevitable feature of natural aging.In the case of heart failure, as recently as the mid-1980s it was believed that little could be done to improve the natural history in patients with advanced chronic heart failure and a severely dilated ventricle.Yet within a few years, work from unexpected directions demonstrated that the progressive deterioration of the failing heart can be slowed and prognosis improved.
Role of the spleen in the peripheral vascular response to severe exercise in untethered dogs
Authors: S. F. VATNER, C. B. HIGGINS, R. W. MILLARD, D. FRANKLIN
Journal: Cardiovascular Research (1974)

Journal Article Role of the spleen in the peripheral vascular response to severe exercise in untethered dogs Get access STEPHEN F. VATNER, STEPHEN F. VATNER 2 From the Departments of Medicine, Peter Bent Brigham Hospital and Harvard Medical School; the Department of Cardiology, Children's Hospital Medical Center, Boston, Massachusetts; and from the Department of Medicine, University of California, San Diego, California, USA 2Reprint requests to: Stephen F. Vatner, MD, Harvard Medical School, 25 Shattuck Street, Boston, Mass 02115, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar CHARLES B. HIGGINS, CHARLES B. HIGGINS From the Departments of Medicine, Peter Bent Brigham Hospital and Harvard Medical School; the Department of Cardiology, Children's Hospital Medical Center, Boston, Massachusetts; and from the Department of Medicine, University of California, San Diego, California, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar RONALD W. MILLARD, RONALD W. MILLARD From the Departments of Medicine, Peter Bent Brigham Hospital and Harvard Medical School; the Department of Cardiology, Children's Hospital Medical Center, Boston, Massachusetts; and from the Department of Medicine, University of California, San Diego, California, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar DEAN FRANKLIN DEAN FRANKLIN From the Departments of Medicine, Peter Bent Brigham Hospital and Harvard Medical School; the Department of Cardiology, Children's Hospital Medical Center, Boston, Massachusetts; and from the Department of Medicine, University of California, San Diego, California, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 8, Issue 2, March 1974, Pages 276–282, https://doi.org/10.1093/cvr/8.2.276 Published: 01 March 1974
In vivo single-photon emission computed tomography imaging of apoptosis in Crohn's disease and anti-tumour necrosis factor therapy
Authors: A. J M Watson
Journal: Gut (2007)

It has long been known that apoptosis of T cells is an important mechanism for terminating inflammatory reactions.1 It was proposed over 10 years ago that defective apoptosis could play a role in the pathogenesis of inflammatory bowel disease.2 There is now substantial experimental and clinical evidence supporting this hypothesis.3

In Crohn’s disease there is an expansion in CD4 T-cell populations mediated by tumour necrosis factor (TNF) and γ-interferon (IFN-γ), which activate macrophages to release interleukin-6, interleukin-12 and TNF.4,5 These cytokines act to perpetuate the inflammatory reaction by reducing the susceptibility of T cells to die by apoptosis.3 In the uninflammed state, lamina propria T cells have a higher susceptibility to apoptosis than unstimulated T cells from the peripheral blood because of high expression of the apoptosis-inducing receptor Fas.6 In contrast to this, lamina propria T cells from patients with Crohn’s disease are resistant to apoptotic stimuli.7 These observations suggest that apoptosis limits the number of CD4 T cells in healthy individuals whereas in Crohn’s disease expansion of T-cell populations can occur without the restriction of apoptosis.

This resistance to induction of apoptosis is mediated by interleukin-12, the interleukin-6 receptor and TNF. Interleukin-12 is one of the most important cytokines in Crohn’s disease promoting Th1 T-cell differentiation. It also renders T cells resistant to Fas-induced apoptosis, possibly through inhibition of caspase 3 and 9, thereby prolonging T-cell survival.8 Early clinical studies have shown that antibodies that block the action of interleukin-12 reduce the severity of Crohn’s disease.9 Such antibodies also increase apoptosis in lamina propria T cells and reduce the severity of trinitrobenzene sulphonic acid experimental colitis.5

Interleukin-6 secreted by lamina propria macrophages and T cells also promotes the survival of T cells by inhibiting …