tbuckley/cabot-search huggingface dataset:
6-year follow-up of 522 HIV-positive individuals screened for<i>Mycobacterium tuberculosis</i>infection in Denmark
Authors: Christian Soborg, Morten Ruhwald, Peter H. Andersen, Pernille Ravn
Journal: European Respiratory Journal (2014)

To the Editor: 

We report the result of a 6-year follow-up study among 522 HIV-positive patients showing a positive predictive value (PPV) of 7% (two out of 28) and a negative predictive value (NPV) of 100% (478 out of 478) for developing active tuberculosis (TB) using the QuantiFERON-TB Gold In-Tube test (QFT-IT).

Denmark is a low TB incidence country with an annual incidence rate of six cases per 100 000 persons and a HIV prevalence of 70 cases per 100 000 persons [1]. Among HIV-positive patients registered in the Danish HIV Cohort, comprising all known HIV-positive individuals in Denmark, the incidence rate of TB was as high as 8.2 cases per 1000 person-years [2]. The rate was highest before and within the first 6 months of antiretroviral treatment (ART) and among patients with known TB risk factors.

HIV is a well-known risk factor for developing active TB, increasing the risk >20-fold compared to HIV-uninfected individuals [3–5]. In Eastern Europe the risk of death in HIV patients co-infected with TB is especially high [6].

Isoniazid preventive treatment (IPT) has shown to be effective in preventing reactivation of TB in HIV positive individuals [7–9], and the treatment has been recommended by the World Health Organization and the US Centers for Disease Control and Prevention [10].

In order to prevent further spread of the disease and prevent infection, IPT of HIV-positive individuals is now recommended in high-burden regions, independently of tuberculin skin test or interferon-gamma release assay results [10].

In Denmark, screening and treatment of latent TB infection is only recommended in individuals with recent TB exposure and candidates of tumour necrosis factor (TNF)-α inhibitor treatment, but no specific guidelines exist for HIV-positive individuals.

The …
TMPRSS2-ERG Status in Circulating Tumor Cells as a Predictive Biomarker of Sensitivity in Castration-Resistant Prostate Cancer Patients Treated With Abiraterone Acetate
Authors: Daniel C. Danila, Aseem Anand, Clifford C. Sung, Glenn Heller, Margaret A. Leversha, Long Cao, Hans Lilja, Arturo Molina, Charles L. Sawyers, Martin Fleisher, Howard I. Scher
Journal: European Urology (2011)
Non-imprinted allele-specific DNA methylation on human autosomes
Authors: Yingying Zhang, Christian Rohde, Richard Reinhardt, Claudia Voelcker-Rehage, Albert Jeltsch
Journal: Genome biology (2009)

Abstract Background Differential DNA methylation between alleles is well established in imprinted genes and the X chromosomes in females but has rarely been reported at non-imprinted loci on autosomes. Results We studied DNA methylation of cytosine-guanine dinucleotide (CpG) islands on chromosome 21 in leukocytes from several healthy individuals and observed novel cases of pronounced differential methylation of alleles. Allele-specific methylation affected complete CpG islands with methylation differences between alleles of up to 85%. The methylation differences between alleles were strongly correlated with the genotypes, excluding a connection to imprinting. We show that allele-specific methylation can lead to allelic repression of the methylated gene copy. Based on our results, allele-specific methylation is likely to affect about 10% of all human genes and to contribute to allele-specific expression and monoallelic gene silencing. Therefore, allele-specific methylation represents an epigenetic pathway of how genetic polymorphisms may lead to phenotypic variability. In most cases, we observed that some, but not all, heterozygous individuals showed allele-specific methylation, suggesting that allele-specific methylation is the outcome of an epigenetic drift, the direction of which is determined by the genetic differences between the alleles. We could show that the tendency to acquire hypermethylation in one allele was inherited. Conclusions We observed that larger differences in methylation levels between individuals were often coupled to allele-specific methylation and genetic polymorphisms, suggesting that the inter-individual variability of DNA methylation is strongly influenced by genetic differences. Therefore, genetic differences must be taken into account in future comparative DNA methylation studies.
Rescue of the colony-stimulating factor 1 (CSF-1)–nullizygous mouse (Csf1op/Csf1op) phenotype with a CSF-1 transgene and identification of sites of local CSF-1 synthesis
Authors: Gregory R. Ryan, Xu-Ming Dai, Melissa G. Dominguez, Wei Tong, Fenchi Chuan, Orin Chisholm, Robert G. Russell, Jeffrey W. Pollard, E. Richard Stanley
Journal: Blood (2001)
Trends in Tuberculosis Transmission
Authors: Richard J. Blinkhorn
Journal: Annals of Internal Medicine (2000)

Letters7 March 2000Trends in Tuberculosis TransmissionRichard J. Blinkhorn Jr, MDRichard J. Blinkhorn Jr, MDMetrohealth Medical Center; Cleveland, OH 44109 (Blinkhorn)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-132-5-200003070-00013 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Jasmer and colleagues (1) may be overestimating the role of molecular epidemiologic analysis in tuberculosis control. The tuberculosis control measures that were reportedly intensified appear to represent well-known traditional principles and arguably should have been in place already. Could it not be argued that the only variable truly affecting clustering of tuberculosis cases was the decline in HIV-tuberculosis co-infection? The local rate of HIV-infected patients with tuberculosis decreased to 16% in 1996 and 5% in 1997. What percentage of clustered cases involved HIV-infected persons? Although DNA fingerprinting enables us to assign individual cases of tuberculosis to clusters, ...Reference1. Jasmer RM, Hahn JA, Small PM, Daley CL, Behr MA, Moss AR, et al . A molecular epidemiologic analysis of tuberculosis trends in San Francisco, 1991-1997. Ann Intern Med. 1999;130:971-8. LinkGoogle Scholar Author, Article, and Disclosure InformationAffiliations: Metrohealth Medical Center; Cleveland, OH 44109 (Blinkhorn) PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoA Molecular Epidemiologic Analysis of Tuberculosis Trends in San Francisco, 1991–1997 Robert M. Jasmer , Judith A. Hahn , Peter M. Small , Charles L. Daley , Marcel A. Behr , Andrew R. Moss , Jennifer M. Creasman , Gisela F. Schecter , E. Antonio Paz , and Philip C. Hopewell Trends in Tuberculosis Transmission Robert M. Jasmer , Charles L. Daley , and Philip C. Hopewell Metrics 7 March 2000Volume 132, Issue 5Page: 416KeywordsDirectly observed therapyGenetic fingerprintingMolecular epidemiologySputum Issue Published: 7 March 2000 CopyrightCopyright © 2000 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
338 ONCOLYTIC VIROTHERAPY AND THE PROTEASOME INHIBITOR BORTEZOMIB ACT SYNERGISTICALLY IN THE TREATMENT OF HEPATOCELLULAR CARCINOMA
Authors: B. Boozari, T.C. Wirth, N. Woller, M.P. Manns, S. Kubicka, F. Kuehnel
Journal: Journal of Hepatology (2008)
Hyperlipemia During Estrogen Therapy
Authors: Joel E. Bernstein
Journal: JAMA (1974)

<h3>To the Editor.—</h3> In both cases, the subjects had histories of hypertension preceding estrogen therapy, had diabetes mellitus, and had strong family histories of atherosclerotic vascular disease (as well as a family history of diabetes mellitus and hypercholesterolemia in one case). Additionally, one of the patients was known to have had hyperlipemia seven years prior to initiation of estrogen therapy, while the other was first shown to have hyperlipemia four months after she had discontinued a short course of conjugated estrogen therapy. Thus, any hypothesis with respect to the estrogen-provoking hyperlipemia is extremely doubtful in these two women. The authors consider their strongest evidence for the relationship of hyperlipemia with estrogen treatment to be the decrease in plasma lipid levels after cessation of estrogens. However, it is stated that both subjects were initially on a low-carbohydrate, low-saturated-fat reducing diet after discovery of their hyperlipemia. Thus, the improvement can be directly
Cause-specific mortality and second cancer incidence after non-Hodgkin lymphoma: a report from the Childhood Cancer Survivor Study
Authors: Elizabeth C. Bluhm, Cécile Ronckers, Robert J. Hayashi, Joseph P. Neglia, Ann C. Mertens, Marilyn Stovall, Anna T. Meadows, Pauline A. Mitby, John A. Whitton, Sue Hammond, Joseph D. Barker, Sarah S. Donaldson, Leslie L. Robison, Peter D. Inskip
Journal: Blood (2008)
Talwin 50 reformulated to avert 'T's and blues' abuse
Authors: Carla Carlson
Journal: JAMA (1983)

In a move to reduce illegal use of the oral prescription analgesic Talwin 50, Winthrop Laboratories, a division of Sterling Drug Inc., has reformulated the drug so that if taken inappropriately, it will give abusers withdrawal-like symptoms rather than a "high." Talwin 50 (pentazocine hydrochloride), when crushed, dissolved together with the blue tablet tripelennamine (an antihistamine), and injected intravenously, provides a high similar to that of heroin (<i>JAMA</i>[MEDICAL NEWS] 1982;247:409). Several years ago, street people began to use the combination, called "T's and blues," as an alternative to costly heroin. The new formulation, which just went on the market, contains 50 mg of pentazocine and 0.5 mg of naloxone. Naloxone, a narcotic antagonist, is inactive when taken by mouth and does not affect the safety and efficacy of pentazocine when taken orally as intended, according to Sterling. However, if the new formulation—called Talwin Nx—is misused and taken intravenously, withdrawal
The Essential Role of Generalists in Health Care Systems
Authors: Robert L. Ferrer, Simon J. Hambidge, Rose C. Maly
Journal: Annals of Internal Medicine (2005)

Viewing primary care as merely one of the many niches in individual patient care fosters a narrow perspective that neither accounts for the full value of primary care nor offers proper guidance for reforming it. Instead, a systems view better articulates primary care's essential role in increasing the effectiveness and efficiency of other health care services. Primary care improves health care system functioning through such services as managing and triaging undifferentiated symptoms, matching patient needs to health care resources, and enhancing the system's ability to adapt to new circumstances. By acting as an appropriate filter for high-technology care, primary care helps ensure that it is appropriately applied, a major determinant of outcomes. Furthermore, because primary care is the most financially and geographically accessible arm of the health care system, it reduces socioeconomic and geographic disparities across the population. Even in the de facto health system that exists in the United States, these functions are necessary for the efficient, equitable, and sustainable delivery of health care and the adaptability and resilience of the system as a whole. As primary care reforms proceed, it will be important to explicitly consider how to support and strengthen its system-level benefits. Needed reforms include enabling universal access to primary care and providing the leadership, training, and infrastructure support to improve its performance as a central hub in the network of patients, clinicians, and communities. It is important that health systems realize the essential integrative function of primary care.
HIV-1 recombinant poxvirus vaccine induces cross-protection against HIV-2 challenge in rhesus macaques
Authors: Alash'le G. Abimiku, Genoveffa Franchini, James Tartaglia, Kristine Aldrich, Maria Myagkikh, Phillip D. Markham, Pele Chong, Michel Klein, Marie-Paule Kieny, Enzo Paoletti, Robert C. Gallo, Marjorie Robert-Guroff
Journal: Nature Medicine (1995)
Prospective Study of Cytomegalovirus Infection in Pregnancy
Authors: H. Stern, S. M. Tucker
Journal: BMJ (1973)

In a prospective study of cytomegalovirus infection in 1,040 pregnant women in London 319 (42%) of the white Englishwomen but only 28 (10%) of the immigrant Asian women were without antibodies at the onset of pregnancy. Out of 254 susceptible white women and 16 susceptible Asian women 8 (3%) and 3 (16%) respectively experienced primary infection during the course of pregnancy. The overall incidence of fetal infection after primary infection in the mother was almost 50%, and was higher in early pregnancy. One out of the five infected infants was found to be mentally retarded. Reactivation of latent infection was recognized in 0·7-2·9% of pregnant women; this occurred without involving the fetus.
Cigarette smoking, gastric acid secretion, and serum pepsinogen I concentrations in duodenal ulcer patients.
Authors: F Parente, M Lazzaroni, O Sangaletti, S Baroni, G Bianchi Porro
Journal: Gut (1985)

Cigarette smoking has been linked with duodenal ulcer disease although the mechanism of this association is unclear. This study assessed basal gastric secretory response to acute smoking of smokers with an active duodenal ulcer; in addition the possible effects of chronic smoking on gastric secretory capacity, as expressed by pentagastrin stimulated gastric acid secretion and fasting serum pepsinogen I (PG I) concentrations, were investigated in patients with active duodenal ulcer, or non-ulcer dyspepsia. In 10 smokers with duodenal ulcer smoking four cigarettes during 40 minutes did not influence basal gastric secretion of acid and pepsin, or serum PG I and gastrin concentrations. In 136 patients with duodenal ulcer and 90 controls with non-ulcer dyspepsia, pentagastrin stimulated acid secretion and fasting serum PG I concentrations were significantly higher among habitual heavy smokers than among non-smokers. These findings suggest that in heavy smokers with duodenal ulcer acid- and pepsin-secreting cell function is not affected by acute cigarette smoking. By contrast, chronic cigarette smoking seems to be associated either with an increase of parietal- and chief-cell mass, or with an enhancement of their secretory capacity.
SETBP1 mutations drive leukemic transformation in ASXL1-mutated MDS
Authors: D Inoue, J Kitaura, H Matsui, H-A Hou, W-C Chou, A Nagamachi, K C Kawabata, K Togami, R Nagase, S Horikawa, M Saika, J-B Micol, Y Hayashi, Y Harada, H Harada, T Inaba, H-F Tien, O Abdel-Wahab, T Kitamura
Journal: Leukemia (2014)
Postgraduate Work in Vienna.
Authors: J. N. Hall
Journal: JAMA (1907)

Vienna, Austria, Nov. 12, 1907. <h3>To the Editor:</h3> —Some readers ofThe Journal, and especially those younger ones who intend to study in Vienna, will perhaps be interested in the observations of an American physician here. There are probably eighty-five American doctors studying here at present. Since my last visit an efficient "American Medical Association of Vienna" has been organized and is of great assistance in helping newcomers to get properly started on their studies. By writing to the secretary of this association at Café Klinik, 21 Spital Gasse IX, Vienna, a pamphlet may be obtained, giving the information in condensed form that an American wishes for in deciding where and how to study abroad. Lectures on some live subject are given frequently by some of the Vienna faculty before the association. The course which many believe to be the best in the world for American students—that on gross pathology
Isolation of Chlamydia pneumoniae from the Coronary Artery of a Patient with Coronary Atherosclerosis
Authors: Julio A. Ramirez
Journal: Annals of Internal Medicine (1996)

Atherosclerosis is pathologically similar to a chronic inflammatory response. Recent reports have suggested that Chlamydia pneumoniae may play a role in the pathogenesis of atherosclerosis.To determine, by using various detection methods, whether C. pneumoniae is present in the coronary arteries of patients with coronary atherosclerosis.Multicenter investigation.The Jewish Hospital Heart and Lung Institute in Louisville, Kentucky, and several laboratories.12 patients seeking heart transplantation.Culture for C. pneumoniae was done in HEp-2 cell monolayers. Other methods of detection included polymerase chain reaction (PCR) assay, immunocytochemistry, transmission electron microscopy, and in situ hybridization.Chlamydia pneumoniae was cultured from atherosclerotic plaques in one patient with severe coronary artery disease. The organism was found in the atheromas of this patient by PCR assay, immunocytochemistry, electron microscopy, and in situ hybridization. In addition, at least one testing method showed C. pneumoniae in coronary artery tissue in six of nine additional patients with coronary atherosclerosis.This study provides direct evidence of the presence of viable C. pneumoniae in atheromatous lesions. A chronic inflammatory response caused by a persistent infection of the coronary arteries may explain the link between C. pneumoniae and atherosclerosis.
Increased myocardial adenosine production and reduction of beta-adrenergic contractile response in aged hearts.
Authors: J G Dobson, R A Fenton, F D Romano
Journal: Circulation Research (1990)

The contractile response of the aged adult heart to beta-adrenergic stimulation is known to be reduced compared with the young adult heart. Since endogenous adenosine exerts an antiadrenergic action in the heart, this study was undertaken to determine if the basal endogenous level of myocardial adenosine increases with age and whether this increase mediates the reduced responsiveness of aged heart to beta-adrenergic stimulation. Young (3-5 months) and aged (12-22 months) Sprague-Dawley adult rat hearts of CD and SD stock were perfused at constant pressure and paced at 270 contractions/min. The two age groups had a similar level of +dP/dtmax (index of contractility) under control conditions. Adenosine release into the coronary effluent was 30 +/- 3 nmol/min/g dry wt from young and 54 +/- 9 nmol/min/g dry wt from aged hearts. Inosine release was also greater from the aged hearts. Isoproterenol (10(-8) M) stimulation increased contractile state by 113% in young hearts and only 69% in aged hearts. Isoproterenol further increased the adenosine and inosine release from both age groups. Theophylline (5 x 10(-5) M), an adenosine antagonist, prevented the difference in the contractile response to isoproterenol stimulation between the young and aged hearts. Elevation of external calcium from 2 to 4 mM increased contractility equally in both age groups without influencing adenosine release. Myocardial oxygen consumption, coronary effluent PO2, oxygen supply-demand ratio, and lactate release were similar for both age groups, indicating that under the conditions studied the elevated release of adenosine by the aged hearts was not due to hypoxia. Aged (10-14 months) adult guinea pig hearts also displayed a reduced responsiveness to the isoproterenol stimulation and released more adenosine compared with young (3-4 months) adult guinea pig hearts. These findings suggest that enhanced adenosine levels that are present in the aged myocardium are responsible, in part, for the reduced contractile responsiveness of the older adult heart to beta-adrenergic stimulation.
Abstract 3100: HOX transcription factors promote cell survival in breast cancer
Authors: Richard Morgan, Agnieszka Michael, Aagna Bhatt, Kevin Harrington, Angela Boxall, Nicola Annels, Hardev Pandha
Journal: Cancer Research (2011)

Abstract The HOX genes are a family of closely related transcription factors that help to define the identity of cells and tissues during embryonic development and which are also frequently deregulated in a number of malignancies, including breast cancer. Whilst relatively little is known about the roles that individual HOX genes play in cancer, it is however clear that these roles can be both contradictory, with some members acting as oncogenes and some as tumour suppressors, and also redundant, with several genes essentially having the same function. Here we have attempted to address this complexity by using the HXR9 peptide to target the interaction between HOX proteins and PBX, a second transcription factor that serves as a common co-factor for many HOX proteins. We show that HXR9 causes apoptosis in a number of breast cancer-derived cell lines and that sensitivity to HXR9 is directly related to the averaged expression of HOX genes HOXB1 through to HOXB9, providing a potential biomarker to predict the sensitivity of breast tumours to HXR9 or its derivatives. Furthermore, we show that whilst HXR9 blocks the oncogenic activity of HOX genes, it does not affect the known tumour-suppressor properties of a subset of HOX genes in breast cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3100. doi:10.1158/1538-7445.AM2011-3100
The degeneration of biological cardiovascular prostheses under pro-calcific metabolic conditions in a small animal model
Authors: Alexander Assmann, Kai Zwirnmann, Friederike Heidelberg, Franziska Schiffer, Kim Horstkötter, Hiroshi Munakata, Felix Gremse, Mareike Barth, Artur Lichtenberg, Payam Akhyari
Journal: Biomaterials (2014)
A specific IgG in Graves' ophthalmopathy and its relation to retro-orbital and thyroid autoimmunity.
Authors: P Kendall-Taylor, S Atkinson, M Holcombe
Journal: BMJ (1984)

An IgG (ophthalmopathic immunoglobulin) that binds to retro-orbital antigen was identified in serum from patients with active Graves9 ophthalmopathy, and its nature and specificity were investigated. Dose related binding of this immunoglobulin to retro-orbital antigens prepared from guinea pig harderian gland or porcine eye muscle was found, which could be abolished by prior incubation with antigen. The immunoglobulin did not bind to thyroid membranes, thyroid microsomes, or thyroglobulin or interact with liver, skeletal muscle, or fat membranes. Serum with high activity of thyrotrophin binding inhibiting immunoglobulin did not react with retro-orbital antigen, and this activity was not affected by preincubation of the serum with retro-orbital antigen. Thyroid stimulating hormone was also without effect on retro-orbital antigen. It is concluded that Graves9 ophthalmopathy is associated with a specific ophthalmopathic immunoglobulin that reacts with retro-orbital antigen as distinct from thyroid antigens, and that the autoimmune response is directed towards retro-orbital antigens. This suggests that the ophthalmopathy is an entity distinct from autoimmune thyroid disease.
Lowering Cholesterol With Granulocyte-Macrophage Colony-Stimulating Factor-Reply
Authors: Stephen D. Nimer
Journal: JAMA (1989)

<h3>In Reply.—</h3> We appreciate the comments of Dr Goldstein and Drs Mazur and Herbert regarding our recent report in<i>JAMA</i>. We have data available on changes in low-density lipoprotein and high-density lipoprotein (HDL) cholesterol concentrations in five of the eight patients reported (Table). In three of these patients HDL-cholesterol decreased slightly, but in all instances the decrease in HDL-cholesterol was proportionally less than the decrease in low-density lipoprotein cholesterol, resulting in a lower low-density lipoprotein/HDL cholesterol ratio. In one of the patients HDL-cholesterol levels increased during GM-CSF therapy and in the other patient there was no real change in HDL-cholesterol levels. The low-density lipoprotein/HDL cholesterol ratios decreased in all patients, a favorable direction in considering the possible treatment or prevention of atherosclerosis with GM-CSF or other factors that use similar mechanisms. Our findings are indeed preliminary, but we are actively exploring the mechanism of action of GM-CSF's cholesterollowering activity. As