tbuckley/cabot-search huggingface dataset:
Rheumatic Fever: Diagnosis, Management and Prevention
Authors: J. W. HOLLINGSWORTH
Journal: JAMA (1965)

Rheumatic fever has been intensively studied clinically over the last half-century. Because of the sequelae of heart valvular scarring and because children are so prominently affected, the disease has commanded exceptional attention from clinical investigators. Since streptococcal infections are important in the pathogenesis of rheumatic fever, microbiologists have joined the effort in recent years. From this intensive clinical and microbiological research has emerged a remarkably complete documentation of the natural history of rheumatic fever, with statistical-clinical correlation of events from the onset of the inciting streptococcal pharyngitis to the progress of the valvular heart disease. Drs. Markowitz and Kuttner have done a remarkable job of synthesizing from many publications a composite picture of rheumatic fever. Their work is not simply scholarly but reflects their years of clinical experience, contemplation and research in rheumatic fever and poststreptococcal disease states. The writing is that of the seasoned and experienced physician, answering the
Mechanistic insights into immunomodulation by hepatic stellate cells in mice: A critical role of interferon-γ signaling
Authors: Horng-Ren Yang, Hong-Shuie Chou, Xiaodong Gu, Lianfu Wang, Kathleen E. Brown, John J. Fung, Lina Lu, Shiguang Qian
Journal: Hepatology (2009)

The liver is considered to be an immune-privileged organ that favors the induction of tolerance. The underlying mechanisms are not completely understood. Interestingly, liver transplants are spontaneously accepted in several animal models, but hepatocyte transplants are acutely rejected, suggesting that liver nonparenchymal cells may effectively protect the parenchymal cells from immune attack. We have shown the profound T cell inhibitory activity of hepatic stellate cells (HSCs). Thus, cotransplantation with HSCs effectively protects islet allografts from rejection in mice. In this study, using T cell receptor transgenic and gene knockout approaches, we provided definitive evidence that HSCs protected cotransplanted islet allografts by exerting comprehensive inhibitory effects on T cells, including apoptotic death in graft-infiltrating antigen-specific effector T cells and marked expansion of CD4(+) Forkhead box protein (Foxp)3(+) T regulatory (Treg) cells. All these effects required an intact interferon-gamma (IFN-gamma) signaling in HSCs, demonstrated by using HSCs isolated from IFN-gamma receptor 1 knockout mice. B7-H1 expression on HSCs, a product molecule of IFN-gamma signaling, was responsible for induction of T cells apoptosis, but had no effect on expansion of Treg cells, suggesting that undetermined effector molecules produced by IFN-gamma signaling is involved in this process.Upon inflammatory stimulation, specific organ stromal cells (such as HSCs in the liver) demonstrate potent immune regulatory activity. Understanding of the mechanisms involved may lead to development of novel strategies for clinical applications in transplantation and autoimmune diseases.
Effect of rheumatoid factor on mortality and coronary heart disease
Authors: G. Tomasson, T. Aspelund, T. Jonsson, H. Valdimarsson, D. T. Felson, V. Gudnason
Journal: Annals of the Rheumatic Diseases (2009)

An association between rheumatoid factor (RF) and increased mortality has been described in individuals with rheumatoid arthritis. The objective of this study was to determine the effect of RF on mortality and coronary heart disease (CHD) in the general population.
The effects of hormonal and other stimuli on cell-surface Ro/SSA antigen expression by human keratinocytes in vitro: their possible role in the induction of cutaneous lupus lesions
Authors: S. K. JONES
Journal: British Journal of Dermatology (2008)

Summary Ultraviolet B light (UVB) has previously been shown to induce the expression of the extractable nuclear antigens (e.g. Ro/SSA) on the surfaces of human keratinocytes in vitro. This study assessed whether injurious, metabolic, inflammatory, immunological or hormonal stimuli would also induce this expression or modulate that produced by UVB. No stimulus initiated expression alone, but 17-β oestradiol doubled that found in response to UVB. These findings confirm the potential role of UVB in the initiation and potentiation of cutaneous lupus lesions and may help to explain the female preponderance of the disease.
Learning by Failing: Ideas and Concepts to Tackle γ-Secretases in Alzheimer's Disease and Beyond
Authors: Bart De Strooper, Lucía Chávez Gutiérrez
Journal: The Annual Review of Pharmacology and Toxicology (2014)

γ-Secretases are a group of widely expressed, intramembrane-cleaving proteases involved in many physiological processes. Their clinical relevance comes from their involvement in Alzheimer's disease, cancer, and other disorders. A clinical trial with the wide-spectrum γ-secretase inhibitor semagacestat has, however, demonstrated that global inhibition of all γ-secretases causes serious toxicity. Evolving insights suggest that selective inhibition of one of these proteases, or more subtle modulation of γ-secretases by stimulating their carboxypeptidase-like activity but sparing their endopeptidase activity, are potentially highly interesting approaches. The rapidly growing knowledge of regulation, assembly, and specificity of these intriguing protein complexes and the potential advent of high-resolution structural information could dramatically change the perspective on safe and efficacious γ-secretase inhibition in various disorders.
FURTHER OBSERVATIONS ON THE RELEVANCE OF SEROLOGIC RECAPITULATIONS OF HUMAN INFECTION WITH INFLUENZA VIRUSES
Authors: F. M. Davenport, A. V. Hennessy, J. Drescher, J. Mulder, T. Francis
Journal: The Journal of Experimental Medicine (1964)

By use of a photometric method which objectively distinguishes between homologous and heterologous antibody reactions, the age distribution of specifically reacting swine and Asian antibodies present in sera of persons not recently exposed to either virus was established. The findings support the thesis that the unique distribution by age of swine and Asian antibodies recognizes two past periods of prevalence of swine and Asian-like viruses, respectively. The findings apparently refute the conclusion that the existence of age-specific Asian and swine antibody patterns is primarily attributable to the undirected or passive accumulation of experience with Asian or swine antigens present as minor antigenic components in most strains of influenza A.
Direct Genetic Correction as a New Method for Diagnosis and Molecular Characterization of MHC Class II Deficiency
Authors: Franck Matheux, Aydan Ikinciogullari, David A. Zapata, Emmanuèle Barras, Madeleine Zufferey, Figen Dogu, José R. Regueiro, Walter Reith, Jean Villard
Journal: Molecular Therapy (2002)

Major histocompatibility complex class II (MHCII) deficiency is a primary immunodeficiency resulting from defects in one of four different MHCII-specific transcription factors—CIITA, RFX5, RFXAP, and RFXANK. Despite this genetic heterogeneity, the phenotypical manifestations are homogeneous. It is frequently difficult to establish a definitive diagnosis of the disease on the basis of clinical and immunological criteria. Moreover, the phenotypical homogeneity precludes unambiguous identification of the regulatory gene that is affected. Identification of the four genes mutated in the disease has now allowed us to develop a rapid and straightforward diagnostic test for new MHCII-deficiency patients. This test is based on direct correction of the genetic defect by transduction of cells from patients with lentiviral vectors encoding CIITA, RFXANK, RFX5, or RFXAP. We have validated this approach by defining the molecular defects in two new patients. The RFXANK vector restored MHCII expression in a T cell line from one patient. The RFXAP vector corrected primary cells (PBL) from a second patient. Molecular analysis confirmed the presence of homozygous mutations in the RFXANK and RFXAP genes, respectively. Direct genetic correction represents a valuable tool for the diagnosis and classification of new MHCII-deficiency patients.
Abstract 1815: Genome-wide analysis of the molecular crosstalk between mitogenic and proinflammatory signaling in breast cancer.
Authors: Hector L. Franco, Anusha Nagari, W. Lee Kraus
Journal: Cancer Research (2013)

Abstract The interplay between mitogenic (e.g., estradiol) and proinflammatory (e.g., TNFα) signaling pathways play key roles in determining the phenotypes and clinical outcomes of breast cancers. Both pathways promote dramatic changes in the transcriptomes of breast cancer cells, as well as downstream cellular effects, but the interplay between these two pathways at the transcriptional level has not yet been analyzed in a comprehensive way across the genome. We have used global nuclear run-on coupled with deep sequencing (GRO-seq), a genomic method that maps the location and orientation of all actively engaged RNA polymerases, to characterize the immediate transcriptional responses of MCF-7 breast cancer cells treated for short durations (40 min.) with either estradiol (E2), TNFα, or both. In addition, we have integrated these data with chromatin immunoprecipitation coupled with deep sequencing (ChIP-seq) for both estrogen receptor alpha (ERα), which mediates E2 signaling, and the p65 subunit of the NF-κB transcription factor, which mediates TNFα signaling. Our results indicate extensive transcriptional interplay between these two signaling pathways, which is observed for a number of classical mitogenic and proinflammatory protein-coding genes. In addition, GRO-seq has allowed us to capture the transcriptional crosstalk at genomic locations encoding for long non-coding RNAs (lncRNAs), a poorly characterized class of RNAs which have been shown to play important roles in cancer outcomes. The synergistic and antagonistic interplay between E2 and TNFα also manifests itself at the level of ERα and p65 binding, which relocalize to new binding sites that are not occupied by either treatment alone. Taken together, our results identify rapid, signal-dependent transcriptional changes that occur during proliferative signaling versus inflammatory signaling and show that these effects are more extensive than previously anticipated. Uncovering the transcriptional landscape of these two important pathways outside of the protein coding regions of the genome may lead to new ways of diagnosing and treating breast cancer. Citation Format: Hector L. Franco, Anusha Nagari, W. Lee Kraus. Genome-wide analysis of the molecular crosstalk between mitogenic and proinflammatory signaling in breast cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1815. doi:10.1158/1538-7445.AM2013-1815
Pneumococcal Immunization: From Policy to Practice
Authors: Benjamin Schwartz
Journal: JAMA (1990)

The importance of<i>Streptococcus pneumoniae</i>as the leading cause of pneumonia requiring hospitalization and a major cause of death among the elderly and other high-risk populations is well documented.<sup>1,2</sup>For the past 12 years, the availability of pneumococcal vaccine has provided an opportunity to reduce substantially the morbidity and mortality of pneumococcal disease, an opportunity that has been largely unrealized. While the Immunization Practices Advisory Committee and other expert panels uniformly recommend pneumococcal immunization for high-risk populations, and have published increasingly inclusive recommendations in 1981, 1984, and 1989,<sup>3-5</sup>only 10% of the target population have been immunized<sup>6</sup>—a painful reminder of the limited impact of public health policy statements on medical practice. Explanations offered for the low utilization of vaccines targeted for adults include a lack of emphasis on preventive care within the medical community, uncertainty among physicians concerning the high-risk conditions for which immunization is recommended, unfounded concerns
Peptic Ulcer, Partial Gastrectomy, and Pulmonary Tuberculosis
Authors: P. A. Thorn, V. S. Brookes, J. A. H. Waterhouse
Journal: BMJ (1956)

The prevalence of coronary heart disease and of respiratory disability has been investigated amongst a sample of 47 men drawn at random from coal-workers in the Rhondda Fach in the 55-64 age group.It was found that 38% of the subjects had coronary heart disease, of whom half presented with positive clinical findings; 34% had " bronchitis "; and 23% had progressive massive fibrosis of pneumoconiossis.The evidence does not suggest any relationship between these three conditions.The maximum voluntary ventilation (indirect) was on average 73 1./min., and decreased by 17.07 + 2.247 1./min.for unit drop in clinical grade of breathlessness.Coronary heart disease was associated with a significant elevation, and bronchitis or progressive pulmonary fibrosis with a significant reduction, of the maximum voluntary ventilation.The response of blood lactic acid to standard exercise was normal in those subjects with coronary heart disease who were judged fit enough to undertake the test.It is concluded that coronary heart disease does not commonly contribute to impaired ventilatory function.It is a pleasure to acknowledge our indebtedness to our colleagues, in particular Dr.
(10) Relapsing polychondritis
Authors: C.D. Calnan
Journal: British Journal of Dermatology (1974)

Journal Article (10) Relapsing polychondritis Get access C.D. Calnan C.D. Calnan St John's Hospital for Diseases of the Skin, London Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 91, Issue s10, 1 July 1974, Page 53, https://doi.org/10.1111/j.1365-2133.1974.tb12513.x Published: 01 July 1974
BMA criticises CQC's "misleading" banding of GPs
Authors: J. Wise
Journal: BMJ (2014)

The Care Quality Commission’s decision to publish information on every general practice in England has been criticised by the British Medical Association as confusing and potentially misleading to patients and for undermining GPs’ morale.

The CQC’s “intelligent monitoring” of general practices includes 38 indicators relating to patients’ experience, care, and treatment (http://bit.ly/11o2HzX). It has said that it will use the data to categorise general practices into one of six priority bands that are based on the proportion of indicators that have been identified as at “risk.” …
The Rim Sign in Acute Cholecystitis
Authors: MICHAEL B. BRACHMAN, M DAVID GOODMAN, ALAN D. WAXMAN
Journal: Clinical Nuclear Medicine (1993)

Nonvisualization of the gallbladder associated with the rim sign of enhanced pericholecystic hepatic activity has been established as a useful and highly specific sign of acute cholecystitis. This study's purpose was to determine the pathophysiologic cause of the rim sign. Thirty- seven surgery-bound patients with a clinical diagnosis of acute cholecystitis were studied. A group of 20 patients with a definite rim sign were compared to a group of 17 patients without a rim sign; all with nonvisualization of the gallbladder. Radionuclide, surgical, and pathologic findings were correlated. In patients with the rim sign and in those without the rim sign, microscopic review of all surgical specimens revealed transmural reaction of the gallbladder wall in 95% and 59% of cases, respectively. The surgeon found inflammation extending beyond the gallbladder wall in 75% of rim sign cases, but in only 35% of case without the rim sign. Liver tissue was attached to the gallbladder specimen in three cases, and the findings support the association of hepatic inflammation with the presence of a rim sign. Pathologic correlation and surgical evidence suggest that the rim sign is caused by the spread of inflammation through the gallbladder wall and into adjacent liver tissue. Transmural reaction is required before the inflammatory process can reach the liver. A high-count, high-intensity technique seems to best demonstrate the rim sign. Once demonstrated, further delayed imaging is unnecessary.
Levosimendan attenuates pulmonary vascular remodeling
Authors: M. Revermann, M. Schloss, A. Mieth, A. Babelova, K. Schröder, S. Neofitidou, J. Buerkl, T. Kirschning, R. T. Schermuly, C. Hofstetter, R. P. Brandes
Journal: Intensive Care Medicine (2011)
Distribution of vitronectin in plasma and liver tissue: Relationship to chronic liver disease
Authors: Junko Kobayashi, Sadako Yamada, Hironaka Kawasaki
Journal: Hepatology (1994)

To clarify the clinical significance of vitronectin, we compared the concentration of plasma vitronectin with serum fibrous markers and liver function test values in patients with chronic liver diseases. We also evaluated the vitronectin content in the liver by means of enzyme-linked immunosorbent assay and the localization of vitronectin in liver tissue with enzyme immunohistochemistry. In chronic liver disease, the concentration of plasma vitronectin was significantly lower than that in healthy controls, being related to the severity of liver disease. The plasma levels of vitronectin showed no correlation to fibrous markers but a significant correlation with those of serum albumin and prothrombin time. On the other hand, the content of vitronectin in liver tissue was significantly increased in chronic liver disease compared with that in normal controls. In the normal liver, vitronectin was observed in the portal area by light microscopy. In chronic hepatitis and cirrhosis, vitronectin was found in the connective tissue around the portal and central veins and in the areas of piecemeal and focal necrosis. These findings suggested that vitronectin is deposited in injured tissue through the process of repair and fibrosis and plays an important role as an adhesive protein. Moreover, the lower levels of plasma vitronectin in chronic liver disease may be due to its decreased synthesis, deposition or both in injured tissue.
OXYGEN IN THE TREATMENT OF ACUTE CORONARY OCCLUSION
Authors: ALVAN L. BARACH
Journal: JAMA (1934)

In a previous communication<sup>1</sup>we reported that the administration of 50 per cent oxygen to certain patients suffering from coronary thrombosis sustained cardiorespiratory function during a critical period and made possible their ultimate recovery. Because the importance of this measure has not been recognized in a number of recent articles and textbooks, further evidence in support of our original conclusions is presented and the technic of oxygen therapy outlined in detail. When a coronary branch is suddenly occluded, the area of myocardium normally supplied by this vessel is abruptly deprived of blood. The function of the affected muscle is impaired because of lack of nutrition, especially through want of the oxygen necessary for normal contraction. If a sufficiently large area is involved, the heart is no longer able to empty itself of the customary volume of blood and the pressure in the auricles and veins increases. Passive congestion is
Superficial carcinoma of the stomach.
Authors: G Machado, J D Davies, A J Tudway, P R Salmon, A E Read
Journal: BMJ (1976)

Nine cases of superficial gastric carcinoma have been detected with upper gastrointestinal endoscopy in Bristol in the past two years. This contrasted with only six cases found from postoperative gastrectomy specimens examined in the previous eight years. It is often difficult to distinguish a superficial carcinoma from a benign ulcer, and endoscopic diagnosis is effective only if multiple biopsy specimens are taken. Endoscopy should also be repeated and multiple specimens taken until the lesion has healed; even malignant ulcers may heal, and any healed area that is depressed with interrupted mucosal folds should be suspected of malignancy. The endoscopic and histological appearances, the age of the patients, and the clinical behaviour of the disease resembled descriptions of the disease, principally from Japan. Superficial gastric carcinoma is probably under-diagnosed in Britain.
A SPECTACULAR CASE OF LIPOMYXOMA
Authors: Herman C. Little
Journal: JAMA (1913)

<h3>History.</h3> —Patient, aged 24, monk, entered the Yale Mission Hospital, Changsha, China, Oct. 23, 1912, with tumor of the left side of the face and neck of ten years' duration. It began as a small nodule just below the angle of the left lower jaw and increased gradually to the size shown in Figures 1 and 2. Until three months ago the skin of the tumor remained intact, and except for a hypersensitiveness of the skin and tension due to the weight of the growth, there was very little pain. Three months ago the skin broke in two places shown in Figure 2, and since then has broken in several other smaller places. <h3>Examination.</h3> —A large, nodular tumor, so heavy that it caused the patient considerable inconvenience, limited all movements of the head and neck, and had to be carried in his arms when he walked and held in his
Echocardiographic prediction of long‐term response to biventricular pacemaker in severe heart failure
Authors: Enis Oguz, Bahadir Dagdeviren, Tuba Bilsel, Osman Akdemir, Izzet Erdinler, Ahmet Akyol, Tanju Ulufer, Tuna Tezel, Kadir Gurkan
Journal: European Journal of Heart Failure (2002)
Suppression of protein degradation in progressive cardiac hypertrophy of chronic aortic regurgitation.
Authors: N M Magid, J S Borer, M S Young, D C Wallerson, C DeMonteiro
Journal: Circulation (1993)

BACKGROUND The heart adapts to the volume overload of aortic regurgitation with dilation and hypertrophy. The development of left ventricular hypertrophy at the protein level is a dynamic process resulting from an imbalance between cardiac protein synthesis and degradation. The objective of the present study was to determine in vivo the relative contributions of cardiac protein synthesis and degradation to the progressive hypertrophy that occurs in response to chronic aortic regurgitation and to compare these with responses earlier in the course of this stress. METHODS AND RESULTS Continuous intravenous infusions of [3H]-leucine were administered 3 days and 1 month after surgical induction of aortic regurgitation and sham operation in rabbits. Total cardiac protein and myosin heavy chain fractional synthesis rates were obtained by analysis of plasma and protein hydrolysate data using [14C]-dansyl chloride assays. Left ventricular growth rates were determined from serial echocardiographic and postmortem left ventricular weight and protein concentration measurements; protein degradation rates were determined by subtraction of growth rates from synthesis rates. CONCLUSIONS In comparison with sham-operated control rabbits, protein fractional synthesis rates were increased at 3 days but not at 1 month after induction of aortic regurgitation Progressive cardiac hypertrophy occurring at 1 month was caused by a decrease in protein fractional degradation rates. An increase in protein synthesis contributes only to the early phase of hypertrophy caused by acute aortic regurgitation, whereas progressive eccentric hypertrophy in chronic volume overload is due to suppression of protein degradation.