tbuckley/cabot-search huggingface dataset:
Toll-like receptor 9 (TLR9) controls B cell differentiation in salivary glands of patients with sjogren's syndrome
Authors: C. Jamin, T. Guerrier, L. Le Pottier, A. Saraux, P. Youinou, J. Pers
Journal: Annals of the Rheumatic Diseases (2010)

Anti-EC antibodies (AECAs) may be pathogenic in vasculitides. Among a wide range of autoAg, they may recognise ATP synthase, a proton transport molecule regulating intracellular pH (pHi) expressed on the surface of ECs. The aim of the current study was to evaluate ATP synthase antigenicity in vasculitides, and anti-ATP …
Cervical Cancer in Yugoslavia. II. Epidemiologic Factors of Possible Etiologic Significance2
Authors: Irving I. Kessler, Živko Kulčar, Anton Zimolo, Matko Grgurević, Marija Strnad, Barbara J. Goodwin
Journal: JNCI Journal of the National Cancer Institute (1974)

Journal Article Cervical Cancer in Yugoslavia. II. Epidemiologic Factors of Possible Etiologic Significance Get access Irving I. Kessler, Irving I. Kessler 4Department of Epidemiology, The Johns Hopkins University School of Hygiene and Public Health, Baltimore, Md. 21205. Search for other works by this author on: Oxford Academic PubMed Google Scholar Živko Kulčar, Živko Kulčar 5Department of Chronic Diseases, Institute of Public Health of Croatia, Zagreb, Yugoslavia. Search for other works by this author on: Oxford Academic PubMed Google Scholar Anton Zimolo, Anton Zimolo 6Departments of Pathology and Gynecology, Zagreb University Medical School, Zagreb. Search for other works by this author on: Oxford Academic PubMed Google Scholar Matko Grgurević, Matko Grgurević 6Departments of Pathology and Gynecology, Zagreb University Medical School, Zagreb. Search for other works by this author on: Oxford Academic PubMed Google Scholar Marija Strnad, Marija Strnad 5Department of Chronic Diseases, Institute of Public Health of Croatia, Zagreb, Yugoslavia. Search for other works by this author on: Oxford Academic PubMed Google Scholar Barbara J. Goodwin Barbara J. Goodwin 5Department of Chronic Diseases, Institute of Public Health of Croatia, Zagreb, Yugoslavia. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 53, Issue 1, July 1974, Pages 51–60, https://doi.org/10.1093/jnci/53.1.51 Published: 01 July 1974 Article history Received: 19 December 1973 Accepted: 10 April 1974 Published: 01 July 1974
THE CHADS2 SCORE PREDICTS ISCHEMIC STROKE IN THE ABSENCE OF ATRIAL FIBRILLATION AMONG PATIENTS WITH CORONARY HEART DISEASE: DATA FROM THE HEART AND SOUL STUDY
Authors: Christine C. Welles, Beeya Na, Mary A. Whooley, Mintu P. Turakhia
Journal: Journal of the American College of Cardiology (2011)
Differences in PO2 and PCO2 between arterial and arterialized earlobe samples
Authors: A Sauty, C Uldry, LF Debetaz, P Leuenberger, JW Fitting
Journal: European Respiratory Journal (1996)

Arterialized ear lobe blood samples have been described as adequate to gauge gas exchange in acute and chronically ill patients. It is a safe procedure, usually performed by medical technicians. We have conducted a prospective study to verify the validity of this method. One hundred and fifteen consecutive adult patients were studied. Blood samples were drawn simultaneously from arterialized earlobe and radial artery. Values of partial pressure of oxygen (PO2) and of carbon dioxide (PCO2) were measured by means of blood gas electrodes. The correlation coefficients between the two samples were 0.928 for PO2 and 0.957 for PCO2 values. In spite of a highly significant correlation, the limits of agreement between the two methods were wide for PO2. Earlobe values of PO2 were usually lower than arterial values, with larger differences in the range of normal arterial PO2. On the other hand, the error and the limits of agreement were smaller for PCO2. We conclude that, in adult patients, arterialized earlobe blood PO2 is not a reliable mirror of arterial PO2.
Human Heart Failure Is Associated With Abnormal C-Terminal Splicing Variants in the Cardiac Sodium Channel
Authors: Lijuan L. Shang, Arnold E. Pfahnl, Shamarendra Sanyal, Zhe Jiao, Jon Allen, Kathrin Banach, John Fahrenbach, Daiana Weiss, W. Robert Taylor, A. Maziar Zafari, Samuel C. Dudley
Journal: Circulation Research (2007)

Heart failure (HF) is associated with reduced cardiac Na + channel (SCN5A) current. We hypothesized that abnormal transcriptional regulation of this ion channel during HF could help explain the reduced current. Using human hearts explanted at the transplantation, we have identified 3 human C-terminal SCN5A mRNA splicing variants predicted to result in truncated, nonfunctional channels. As compared with normal hearts, the explanted ventricles showed an upregulation of 2 of the variants and a downregulation of the full-length mRNA transcript such that the E28A transcript represented only 48.5% ( P &lt;0.01) of the total SCN5A mRNA. This correlated with a 62.8% ( P &lt;0.01) reduction in Na + channel protein. Lymphoblasts and skeletal muscle expressing SCN5A also showed identical C-terminal splicing variants. Variants showed reduced membrane protein and no functional current. Transfection of truncation variants into a cell line stably transfected with the full-length Na + channel resulted in dose-dependent reductions in channel mRNA and current. Introduction of a premature truncation in the C-terminal region in a single allele of the mouse SCN5A resulted in embryonic lethality. Embryonic stem cell–derived cardiomyocytes expressing the construct showed reductions in Na + channel–dependent electrophysiological parameters, suggesting that the presence of truncated Na + channel mRNA at levels seen in HF is likely to be physiologically significant. In summary, chronic HF was associated with an increase in 2 truncated SCN5A variants and a decrease in the native mRNA. These splice variations may help explain a loss of Na + channel protein and may contribute to the increased arrhythmic risk in clinical HF.
RELATIONSHIP OF MIXED LYMPHOCYTE CULTURE RESPONSE TO HL-A HISTOCOMPATIBILITY ANTIGENS
Authors: John S. Thompson, Michael J. Parmely, Ronald J. Flink, Marilyn S. Canady, Charles D. Severson
Journal: The Journal of Experimental Medicine (1972)

The influence of varying degrees of incompatibility for HL-A antigens on one-way mixed lymphocyte cultures (MLC) has been investigated. Reactions have been compared to a simple expression of HL-A antigens, allele compatibility, and a proposal considering the potential influence of antigen matching in relationship to allele compatibility. As expected, HL-A compatibility was associated with nonstimulated cultures, but significant correlation was not observed when incompatibility was expressed in terms of HL-A antigen or allele mismatching. When the relationship of both was considered, however, a second distinctive group was demonstrated that shared one allele plus one antigen of the second allele. Within this group no stimulation, even with augmented culture conditions, was observed in some families. Employing these same criteria, there was no significant difference in the MLC response in those groups that were incompatible for both alleles regardless of the number of matched antigens or the group that shared an allele but differed by both antigens of the second allele. These results support the concept of an intimate relationship between the loci coding for HL-A antigens and mixed culture reactions. They suggest that HL-A haplotype incompatibility acting as a unit is the primary stimulus of the MLC response, and that the immunogenicity of the haplotype also relates to whether or not one antigen is common to the stimulating and responding cell.
Cardiac Angiotensin II Formation in the Clinical Course of Heart Failure and Its Relationship With Left Ventricular Function
Authors: Gian Gastone Neri Serneri, Maria Boddi, Ilaria Cecioni, Simone Vanni, Mirella Coppo, Maria Letizia Papa, Brunella Bandinelli, Iacopo Bertolozzi, Gianluca Polidori, Thomas Toscano, Massimo Maccherini, Pietro Amedeo Modesti
Journal: Circulation Research (2001)

Abstract —In 76 patients with heart failure (HF) (New York Heart Association [NYHA] classes I through IV) and in 15 control subjects, cardiac angiotensin II (Ang II) generation and its relationship with left ventricular function were investigated by measuring aorta–coronary sinus concentration gradients of endogenous angiotensins and in a part of patients by studying 125 I-labeled Ang I kinetics. Gene expression and cellular localization of the cardiac renin-angiotensin system components, the density of AT 1 and AT 2 on membranes and isolated myocytes, and the capacity of isolated myocytes for synthesizing the hypertrophying growth factors insulin-like growth factor-I (IGF-I) and endothelin (ET)-1 were also investigated on 22 HF explanted hearts (NYHA classes III and IV) and 7 nonfailing (NF) donor hearts. Ang II generation increased with progression of HF, and end-systolic wall stress was the only independent predictor of Ang II formation. Angiotensinogen and angiotensin-converting enzyme mRNA levels were elevated in HF hearts, whereas chymase levels were not, and mRNAs were almost exclusively expressed on nonmyocyte cells. Ang II was immunohistochemically detectable both on myocytes and interstitial cells. Binding studies showed that AT 1 density on failing myocytes did not differ from that of NF myocytes, with preserved AT 1 /AT 2 ratio. Conversely, AT 1 density was lower in failing membranes than in NF ones. Ang II induced IGF-I and ET-1 synthesis by isolated NF myocytes, whereas failing myocytes were unable to respond to Ang II stimulation. This study demonstrates that (1) the clinical course of HF is associated with progressive increase in cardiac Ang II formation, (2) AT 1 density does not change on failing myocytes, and (3) failing myocytes are unable to synthesize IGF-I and ET-1 in response to Ang II stimulation.&gt;
Immunological properties of subcellular rat lymphocyte preparations. Primary allogeneic stimulation in vitro by fractions containing Ia (RT1-B), but not RT1-A antigens.
Authors: A Kaldany, C B Carpenter, C A Shadur, K George, A P Lundin, M Suthanthiran, T B Strom
Journal: The Journal of Experimental Medicine (1980)

Rat thymocyte membrane fractions have been prepared which exhibit strain-specific primary mixed-lymphocyte reaction (MLR)-stimulating and Ia (RT1-B) antigenic properties. These preparations lack the antigenicity of classical, serologically-defined RT1-A (Ag-B) antigens, as defined by in vitro serologic assays. Furthermore, after immunization of allogeneic hosts, specific anti-Ia and MLR-blocking antibodies, but not anti-AgB, alloantibodies are elaborated. Thymidine suicide experiments show that the same clones respond to whole cells and the fragments made from those cells, and the response segregates appropriately in F2 progeny as a major histocompatibility complex (RT1)-linked phenomenon. Hence, it is possible to generate Ia-related allogeneic helper signals in primary, as well as secondary, in vitro responses, using subcellular membrane fragments that have restricted expression of RT1-B-, but not RT1-A-, encoded antigens.
Nonhematopoietic mesenchymal stem cells can be mobilized and differentiate into cardiomyocytes after myocardial infarction
Authors: Hiroshi Kawada, Jun Fujita, Kentaro Kinjo, Yumi Matsuzaki, Mitsuyo Tsuma, Hiroko Miyatake, Yukari Muguruma, Kosuke Tsuboi, Yuji Itabashi, Yasuo Ikeda, Satoshi Ogawa, Hideyuki Okano, Tomomitsu Hotta, Kiyoshi Ando, Keiichi Fukuda
Journal: Blood (2004)
Acceptability of Second-Step Treatments to Depressed Outpatients: A STAR*D Report
Authors: Stephen R. Wisniewski, Maurizio Fava, Madhukar H. Trivedi, Michael E. Thase, Diane Warden, George Niederehe, Edward S. Friedman, Melanie M. Biggs, Harold A. Sackeim, Kathy Shores-Wilson, Patrick J. McGrath, Philip W. Lavori, Sachiko Miyahara, A. John Rush
Journal: American Journal of Psychiatry (2007)

Objective: Treatment of major depressive disorder typically entails implementing treatments in a stepwise fashion until a satisfactory outcome is achieved. This study sought to identify factors that affect patients’ willingness to accept different second-step treatment approaches. Method: Participants in the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial who had unsatisfactory outcomes after initial treatment with citalopram were eligible for a randomized second-step treatment trial. An equipoise-stratified design allowed participants to exclude or include specific treatment strategies. Analyses were conducted to identify factors associated with the acceptability of the following second-step treatments: cognitive therapy versus no cognitive therapy, any switch strategy versus any augmentation strategy (including cognitive therapy), and a medication switch strategy only versus a medication augmentation strategy only. Results: Of the 1,439 participants who entered second-step treatment, 1% accepted all treatment strategies, 3% accepted only cognitive therapy, and 26% accepted cognitive therapy (thus, 71% did not accept cognitive therapy). Those with higher educational levels or a family history of a mood disorder were more likely to accept cognitive therapy. Participants in primary care settings and those who experienced a greater side effect burden or a lower reduction in symptom severity with citalopram were more likely to accept a switch strategy as compared with an augmentation strategy. Those with concurrent drug abuse and recurrent major depressive disorder were less likely to accept a switch strategy. Conclusions: Few participants accepted all treatments. Acceptance of cognitive therapy was primarily associated with sociodemographic characteristics, while acceptance of a treatment switch was associated with the results of the initial treatment.
Gender differences in predictors of the decline of renal function in the general population
Authors: Nynke Halbesma, Auke H. Brantsma, Stephan J.L. Bakker, Desiree F. Jansen, Ronald P. Stolk, Dick De Zeeuw, Paul E. De Jong, Ronald T. Gansevoort, None for the PREVEND study group
Journal: Kidney International (2008)
Abnormal Vascular Reactivity in Growth Hormone Deficiency
Authors: Brunella Capaldo, Vincenzo Guardasole, Francesco Pardo, Margherita Matarazzo, Francesca Di Rella, Fabio Numis, Bartolomeo Merola, Salvatore Longobardi, Luigi Saccà
Journal: Circulation (2001)

Background —The reason why patients with growth hormone (GH) deficiency (GHD) are at increased risk for premature cardiovascular death is still unclear. Although a variety of vascular risk factors have been identified in GHD, little is known regarding vascular reactivity and its contribution to premature arteriosclerosis. Methods and Results —We assessed vascular function in 7 childhood-onset, GH-deficient nontreated patients (age 22±3 years, body mass index [BMI] 25±1 kg/m 2 ) and 10 healthy subjects (age 24±0.4 years, BMI 22±1 kg/m 2 ) by using strain gauge plethysmography to measure forearm blood flow in response to vasodilatory agents. The increase in forearm blood flow to intrabrachial infusion of the endothelium-dependent vasodilator acetylcholine was significantly lower in GH-deficient nontreated patients than in control subjects ( P &lt;0.05). Likewise, forearm release of nitrite and cGMP during acetylcholine stimulation was reduced in GH-deficient nontreated patients ( P &lt;0.05 and P &lt;0.002 versus controls). The response to the endothelium-independent vasodilator sodium nitroprusside was also markedly blunted in GH-deficient patients compared with control subjects ( P &lt;0.005). To confirm that abnormal vascular reactivity was due to GHD, we also studied 8 patients with childhood-onset GHD (age 31±2 years, BMI 24±1 kg/m 2 ) who were receiving stable GH replacement therapy. In these patients, the response to both endothelium-dependent and -independent vasodilators, as well as forearm nitrite and cGMP, release was not different from that observed in normal subjects. Peak hyperemic response to 5-minute forearm ischemia was significantly reduced in GH-deficient nontreated patients (17.2±2.6 mL · dL −1 · min −1 , P &lt;0.01) but not in GH-treated patients (24.8±3.3 mL · dL −1 · min −1 ) compared with normal subjects (29.5±3.2 mL · dL −1 · min −1 ). Conclusions —The data support the concept that GH plays an important role in the maintenance of a normal vascular function in humans.
Localisation and semiquantitative assessment of hepatic procollagen mRNA in primary biliary cirrhosis
Authors: C J R Goddard, A Smith, J A Hoyland, P Baird, R F T McMahon, A J Freemont, M Shomaf, N Y Haboubi, T W Warnes
Journal: Gut (1998)

Chronic liver disease is characterised by excessive deposition of collagen and other extracellular matrix proteins, produced mainly, but not exclusively, by activated hepatic stellate cells in the perisinusoidal space. In primary biliary cirrhosis (PBC) fibrosis is concentrated mainly around the portal tracts.To examine the hypothesis that, in addition to hepatic stellate cells, portal tract fibroblasts might play a significant role in the deposition of collagen in PBC.Fifty liver biopsy specimens from patients with PBC were studied. An in situ hybridisation technique was adapted to localise and measure semiquantitatively type I procollagen mRNA in formalin fixed, paraffin wax embedded sections, using an 35S labelled cRNA probe specific for the alpha 1 chain of rat type I procollagen. Hepatic fibrogenic activity was also assessed using serum type III procollagen peptide (PIIINP).In PBC, type I procollagen gene expression was significantly increased. Signal was localised mainly in and around inflamed portal tracts, to cells which had the appearances of portal fibroblasts. Signal activity in these cells correlated with the degree of portal fibrosis and inflammation and also with serum PIIINP concentrations.Results are consistent with the hypothesis that the excessive extracellular matrix, deposited within the liver in PBC, is synthesised not only by hepatic stellate cells but also by portal tract fibroblasts. The semiquantitative assessment of procollagen mRNA in liver biopsy specimens may provide a useful method of evaluating the rate of synthesis of collagen and therefore disease activity in patients with PBC.
NKp46-mediated killing of human and mouse hepatic stellate cells attenuates liver fibrosis
Authors: Chamutal Gur, Sarit Doron, Shlomit Kfir-Erenfeld, Elad Horwitz, Lina Abu-tair, Rifaat Safadi, Ofer Mandelboim
Journal: Gut (2011)

<h3>Background</h3> Liver fibrosis, which involves activation of hepatic stellate cells (HSC), is a major health problem and is the end outcome of all chronic liver diseases. The liver is populated with lymphocytes, among which are natural killer (NK) cells, whose activity is controlled by inhibitory and activating receptors. NKp46, one of the major NK activating receptors expressed by NK cells, is also a specific NK marker that discriminates NK cells from all other lymphocyte subsets. It recognises viral haemagglutinins and unknown cellular ligands. <h3>Methods</h3> The anti-fibrotic activity of the NKp46 receptor was assessed in vivo and in vitro using NKp46-deficient mice (NCR1<sup>gfp/gfp</sup>), the carbon tetrachloride model and in vitro NK killing assays. Primary murine and human HSC were stained for the expression of the NKp46 ligand using fusion proteins composed of the extracellular portions of the murine and human NKp46 receptors fused to human IgG1. <h3>Results</h3> It was shown that murine HSC express a ligand for the murine orthologue of the NKp46 receptor, NCR1. NCR1 inhibited liver fibrosis in vivo; in vitro, murine HSC were killed in an NCR1-dependent manner. In humans it was shown that human HSC also express a ligand for the human NKp46 receptor and that the killing of human HSC is NKp46 dependent. <h3>Conclusions</h3> In addition to NKG2D, NKp46/NCR1 play an important role in inhibition of liver fibrosis. This suggests that fibrosis can be better controlled through the manipulation of NKp46 activity.
Human Papillomavirus and Rising Oropharyngeal Cancer Incidence in the United States
Authors: Anil K. Chaturvedi, Eric A. Engels, Ruth M. Pfeiffer, Brenda Y. Hernandez, Weihong Xiao, Esther Kim, Bo Jiang, Marc T. Goodman, Maria Sibug-Saber, Wendy Cozen, Lihua Liu, Charles F. Lynch, Nicolas Wentzensen, Richard C. Jordan, Sean Altekruse, William F. Anderson, Philip S. Rosenberg, Maura L. Gillison
Journal: Journal of Clinical Oncology (2011)

Recent increases in incidence and survival of oropharyngeal cancers in the United States have been attributed to human papillomavirus (HPV) infection, but empirical evidence is lacking.
Review of hepatic imaging and a problem-oriented approach to liver masses
Authors: William F. Bennett, James G. Bova
Journal: Hepatology (1990)

We believe that imaging of the liver is complicated. The sporadic appearance of incidental benign lesions and variability in scanning techniques, equipment and artifacts add difficulties to the evaluation of liver masses. Therefore we emphasize the need to define the problem for which the patient is being imaged. This information helps in choosing the procedure of choice and the technique needed to give the most expedient, accurate answer. This will also help apply the lowest risk and most cost-efficient care. Imaging algorithms vary depending on the suspected pathological conditions. Dynamic bolus-enhanced CT is the modality of choice in most situations. Tc99m sulfur-colloid liver-spleen scans are helpful in patients with suspected FNH, and Tc99m-tagged-RBC-SPECT scans are recommended to confirm cavernous hemangiomas. Cysts are easily confirmed by US. Although MRI is competitive with CT, it has not become a primary modality because of cost, availability, patient selection and variability of scanner capabilities among the many manufacturers and models. It is hard to predict what future development of imaging techniques will bring. Many feel that significant advances have plateaued. Time and money will more likely be concentrated on improving image resolution, speed of scanning and ability to transfer this information to sites outside of the radiology department. In addition to faster scanning, we expect to soon have available safe intravenous and enteric contrast agents for MRI. Certainly this will lead to a new round of investigations to compare MRI with CT scanning.
In vivo bradykinin B2 receptor activation reduces renal fibrosis
Authors: Joost P. Schanstra, Eric Neau, Pascale Drogoz, Miguel A. Arevalo Gomez, José Miguel Lopez Novoa, Denis Calise, Christiane Pecher, Michael Bader, Jean-Pierre Girolami, Jean-Loup Bascands
Journal: Journal of Clinical Investigation (2002)

Angiotensin-converting enzyme (ACE) inhibitors reduce the progression of various fibrotic renal diseases both in humans and in animal models. Unilateral ureteral obstruction (UUO) is an animal model of accelerated renal tubulointerstitial fibrosis that is attenuated by ACE inhibition. Although ACE inhibitors increase bradykinin concentrations in addition to their effect on angiotensin II formation, the role of bradykinin in renal fibrosis has not been studied. We show here that genetic ablation (B2(-/-) mice) or pharmacological blockade of the bradykinin B2 receptor increases UUO-induced interstitial fibrosis in mice, whereas transgenic rats expressing increased endogenous bradykinin show reduced UUO-induced interstitial fibrosis. The increased interstitial fibrosis in B2(-/-) mice was accompanied by a decreased activity of plasminogen activators (PAs) and metalloproteinase-2 (MMP-2), enzymes involved in ECM degradation, suggesting that the protective effects of bradykinin involve activation of a B2 receptor/PA/MMP-2 cascade. This ability of bradykinin to increase PA activity was confirmed in primary culture proximal tubular cells. Thus, in both mice and rats, bradykinin B2 receptor activation reduces renal tubulointerstitial fibrosis in vivo, most likely by increasing ECM degradation.