tbuckley/cabot-search huggingface dataset:
Myocardial metabolic changes in experimental non-hypertrophied and hypertrophied right ventricular failure
Authors: Céline Dewachter, Asmae Belhaj, Benoit Rondelet, Robert Naeije, Laurence Dewachter
Journal: European Respiratory Journal (2014)

Metabolic shift toward glycolysis has been implicated in the development of RV dysfunction. We recently reported on experimental models of acute and chronic RV failure both related to RV activation of apoptosis and inflammation, but with variable RV hypertrophy.

We sought to evaluate and compare the expressions of genes implicated in energy substrate use in these models of non-hypertrophied and hypertrophied RV failure.

RV failure was induced by 1) a transient (90-min) pulmonary artery ensnarement in dogs, or by 2) a prolonged (six-month) overcirculation-induced pulmonary arterial hypertension in piglets. Hemodynamics was finally evaluated and RV free wall was sampled for pathobiological evaluation.

In both models, RV presented with decreased expressions of α1, 2-subunits AMP-activated protein kinase, a key cellular energy sensor. Expressions of enzymes implicated in fatty acid oxidation, including carnitine palmitoyltransferase(CPT)-1A and -1B and sterol regulatory element binding transcription factor(SREBF)-1 and -2 decreased in the RV. This was associated with decreased RV expressions of genes implicated in fatty acid oxidation regulation, the peroxisome proliferator-activated receptor(PPAR)-α/PPAR-γ coactivator (PGC)-1 α in the RV. However, expressions of enzymes implicated in glycolytic pathways, including glucose transporter (GLUT1) and glucose-phosphorylating hexokinase-1, increased in hypertrophied dysfunctional RV, while they did not change in non-hypertrophied one.

Acute and chronic afterload-induced RV failure is associated with altered RV fatty acid metabolism, while molecules implicated in glucose uptake are upregulated in the hypertrophied failing RV only.
Can pedometer step count predict severe physical inactivity in COPD
Authors: Claire M. Nolan, Jane L. Canavan, Samantha S.C. Kon, Sarah E. Jones, Michael I. Polkey, William D.-C. Man
Journal: European Respiratory Journal (2013)

Introduction:  Accelerometer measured physical inactivity predicts mortality in COPD (Waschki et al., 2011). Although pedometers may not precisely record step count in slow walking COPD patients, they are cheaper than accelerometers and may detect meaningful physical activity.   Aim:  To identify whether daily pedometer step count can identify severe physical inactivity in COPD.   Method:  36 successive COPD patients consented to wear a pedometer (YamaxDigiwalker®CW700) and acclerometer (Sensewear®) concurrently for one week. Physical activity level (PAL) was calculated from accelerometers. The relationship between daily pedometer step count and PAL was assessed using Spearman’s correlation. Receiver Operator Characteristic plots were used to identify if daily pedometer step count could predict PAL   Results:  Baseline characteristics: 26M/10F; age 69±7.9 years; FEV1 48.1±18%; incremental shuttle walk 227.8±138.7m; COPD Assessment Tool 21.5±7.0; daily pedometer step count 3129±2626; PAL 1.42±0.2. There was a significant correlation between daily pedometer step count and PAL (r=0.58, p   Conclusion:  Pedometers are a simple way of identifying severe physical inactivity in COPD.
Exercise test as preoperative predictor before pulmonary resection surgery
Authors: Ruth Diez, Nuria Marina, Elena Lopez Santa Maria, Maria Alfonso, Juan B. Galdiz
Journal: European Respiratory Journal (2012)

Exercise test (V02) before pulmonary resection surgery was incorporated into the new guidelines (A.Brunell Eur Respir J 2009; 34: 17-41) in the case that the patient presents a FEV 1 and/or TlCO   Material and methods: prospective descriptive study, three months, which included 48 patients evaluated for possible lung resection due to lung neoplasm who presented values less than 80% in the FEV1 or TlCO and preformed a maximum exercise testing to complete the preoperative assessment. Results: mean age (65±8 years); 41 M, 7F. According to the retrieved V02 patients were divided in 3 groups and comparing the values of the FEV 1 and TlCO in each group Table I.  25 patients presented a DLCO and FEV1%   20. Correlations between FEV1 vs VO2 (0,478,P   28/48 patients were operated and in the postoperative follow up(1 month) there was no death and 8 (28.5%) of them had postoperative complications(2 empyema 2 hemothorax,1 fistula 2 pneumonia.,1respiratory failure) These patients presented the following functional parameters FEV1 1686ml, DLCO 51.8%, 17.4 ml/kg/min V02.Conclusions: Patients with mechanical and/or decreased gas exchange (
Plasmacytoid dendritic cells promote HIV-1–induced group 3 innate lymphoid cell depletion
Authors: Zheng Zhang, Liang Cheng, Juanjuan Zhao, Guangming Li, Liguo Zhang, Weiwei Chen, Weiming Nie, Natalia J. Reszka-Blanco, Fu-Sheng Wang, Lishan Su
Journal: Journal of Clinical Investigation (2015)

Group 3 innate lymphoid cells (ILC3s) have demonstrated roles in promoting antibacterial immunity, maintaining epithelial barrier function, and supporting tissue repair. ILC3 alterations are associated with chronic inflammation and inflammatory disease; however, the characteristics and relevant regulatory mechanisms of this cell population in HIV-1 infection are poorly understood due in part to a lack of a robust model. Here, we determined that functional human ILC3s develop in lymphoid organs of humanized mice and that persistent HIV-1 infection in this model depletes ILC3s, as observed in chronic HIV-1-infected patients. In HIV-1-infected mice, effective antiretroviral therapy reversed the loss of ILC3s. HIV-1-dependent reduction of ILC3s required plasmacytoid dendritic cells (pDCs), IFN-I, and the CD95/FasL pathway, as targeted depletion or blockade of these prevented HIV-1-induced ILC3 depletion in vivo and in vitro, respectively. Finally, we determined that HIV-1 infection induces CD95 expression on ILC3s via a pDC- and IFN-I-dependent mechanism that sensitizes ILC3s to undergo CD95/FasL-mediated apoptosis. We conclude that chronic HIV-1 infection depletes ILC3s through pDC activation, induction of IFN-I, and CD95-mediated apoptosis.
A Case Report-The Diagnostic Treatment by Imatinib Led to Curative Resection of Intestinal Gist
Authors: Kazuma Kobayashi, Fumihiko Fujita, Yasuhiro Torashima, Shigeki Minami, Kengo Kanetaka, Mitsuhisa Takatsuki, Takuya Honda, Tamotsu Kuroki, Kazuto Ashizawa, Susumu Eguchi
Journal: Annals of Oncology (2014)
Diversity of human papillomavirus in the anal canal of men: the HIM Study
Authors: L. Sichero, A.G. Nyitray, E.M. Nunes, B. Nepal, S. Ferreira, J.S. Sobrinho, M.L. Baggio, L. Galan, R.C. Silva, E. Lazcano-Ponce, A.R. Giuliano, L.L. Villa
Journal: Clinical Microbiology and Infection (2015)
Factors Involved in Concanavalin A Agglutination of KB and NC37 Cells Grown in Suspension Culture 2
Authors: Betty Altenburg, Sheldon Steiner
Journal: JNCI Journal of the National Cancer Institute (1976)

Journal Article Factors Involved in Concanavalin A Agglutination of KB and NC37 Cells Grown in Suspension Culture Get access Betty Altenburg, Betty Altenburg Search for other works by this author on: Oxford Academic PubMed Google Scholar Sheldon Steiner Sheldon Steiner 3Department of Virology and Epidemiology, Baylor College of Medicine, Houston, Tex. 77025. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 56, Issue 1, January 1976, Pages 197–200, https://doi.org/10.1093/jnci/56.1.197 Published: 01 January 1976 Article history Received: 29 July 1975 Accepted: 12 August 1975 Published: 01 January 1976
Radiation pneumonitis; early diagnosis and associated factors
Authors: Samantha Aso, Susana Padrones, José Ignacio Martínez, Noelia Cubero, Rosa Lopez, Raquel Pascual, Arturo Navarro, Felipe Cardenal, Ana Montes, Jordi Dorca, Federico Manresa, María Molina
Journal: European Respiratory Journal (2014)

Background and aim: radiotherapy (RT) is essential in the treatment of non small cell lung cancer (NSCLC). However, lung radiosensitivity is the main limitation. The aim of this study was to evaluate the incidence of radiation pneumonitis and possible markers for early detection  Methods: 14 patients with NSCLC treated with chemotherapy-radiotherapy were enrolled in a prospective study between 2011 and 2013. Anthropometric values, lung function, tumor features and RT dosimetric data were collected. Bronchoalveolar lavage (BAL) was performed in both lungs before RT and at the third week of treatment. Radiation pneumonitis was scored according the “Common Terminology Criteria for Adverse Events v4.0”. Patients with pneumonitis grade 1 and 3 were selected to perform the molecular analysis by using “Human Cytokine Array Panel A” (R&D Systems).  Results: 35.75% of the patients had pneumonitis grade 1, 20% grade 2, 35.75% grade 3 and 6.66% grade 4. 4 patients developed pneumonitis in the lung without tumour. Lung diffusion capacity for carbon monoxide (DLCO) was the most sensitive parameter for determining the existence of early lung damage (p=0.04). Development of radiation pneumonitis was not associated with lung function or dosimetric data. BAL protein expression before RT differs from the lung that develops grade 1 pneumonitis and grade 3. In both cases, RT induces changes in bilateral BAL protein expression, mainly PAI-1, IL-1ra, MIF, and CXCL-1.  Conclusion: Incidence of radiation pneumonitis is greater than previously reported. DLCO is the most sensitive parameter for its early detection. Risk could have a relationship with the basal lung biomolecular condition. RT induces biological changes in both lungs.
Failure of Hypoxic Pulmonary Vasoconstriction in the Canine Asthma Model
Authors: Martin A. Cohn, Horst Baier, Adam Wanner
Journal: Journal of Clinical Investigation (1978)

Measurements of respiratory mechanics, arterial blood gases, and pulmonary vascular resistance were made before and 15 min after inhalation challenge with Ascaris suum extract in dogs with natural sensitivity to this antigen. 25 of 47 dogs were treated before inhalation challenge with a prostaglandin inhibitor (90 mg/kg of aspirin or 2 mg/kg of indomethacin by intravenous infusion). In response to the challenge, bronchospasm developed in approximately half (responders) of each group reflected by decreases in mean specific respiratory system conductance and arterial oxygen tension. While the dogs were breathing room air, pulmonary vascular resistance remained unchanged after antigen challenge in the responders not given aspirin or indomethacin, but increased significantly and was associated with a lesser degree of arterial hypoxemia in the responders pretreated with either of the prostaglandin inhibitors. Prevention of arterial hypoxemia by oxygen breathing blocked an increase in pulmonary vascular resistance in four pretreated responders. No changes in respiratory mechanics, pulmonary hemodynamics, or arterial blood gases were noted in the 21 dogs who did not develop bronchospasm regardless of whether or not they were pretreated. 12 additional dogs in whom arterial hypoxemia was produced by 10% oxygen breathing, showed an increase in pulmonary vascular resistance that was not potentiated by pretreatment with aspirin in 6. We conclude that in acute experimental canine asthma, vasodilator prostaglandins appear to blunt the hypoxic pulmonary vasoconstrictor response, thereby further compromising gas exchange but preventing the development of pulmonary hypertension.
Evaluation of aldehyde dehydrogenase 1 (ALDH1) as a marker of non-small cell lung cancer (NSCLC) stem cells (SCs) and correlation with prognosis
Authors: R. Zhou, Q. Liu, N. W. Todd, J. Deepak, Z. Liu, S. A. Stass, M. J. Edelman, R. L. Katz, F. Jiang
Journal: Journal of Clinical Oncology (2009)

11105 Background: ALDH1 is a cytosolic enzyme responsible for oxidizing intracellular aldehydes, and conversion of retinol to retinoic acid in SCs. ALDH1 has been previously demonstrated to be a marker for SCs in breast cancer (Ginestier C, et al., Cell Stem Cell. 2007 Nov; 1(5):555–67). The Aldefluor assay is based on conversion of a synthetic substrate BAAA, when passively infused into cytosol, to brightly fluorescent BAA by ALDH1. Combined with fluorescence-activated cell sorting (FACS), it has been used successfully in hematopoietic and breast cancer SCs isolation. ALDH1 is also found in NSCLC. We hypothesized that ALDH1 would be a marker for NSCLC SCs and a potential prognostic marker. Methods: NSCLC SCs were isolated from human NSCLC cell lines using the Aldefluor assay and FACS. ALDH1-positive cells were analyzed extensively for SC characteristics. ALDH1 expression in 303 NSCLC biopsy specimens from three independent cohorts of NSCLC patients was then analyzed by immunohistochemisty (IHC) using an ALDH1 antibody (Santa Cruz Biotechnology) and commercially available negative controls. Results: Isolated cancer cells with high ALDH1 activity displayed cancer SCs features, including capacities for proliferation, self-renewal, differentiation; resistance to chemotherapeutic agents including cisplatin, vinorelbine, gemcitabine and docetaxel; expression of the SC surface marker CD133, and high invasiveness. ALDH1-positive cells generated tumors in vivo recapitulating heterogeneity of parental cells. Xenograft tumors derived from ALDH1-positive cells (10 3 each) were 36±2.9 mm 3 on average in size, with some of the cells having lost ALDH1 expression. Xenograft tumors derived from ALDH1-negative cells (10 5 each) were 4 mm 3 on average in size, without ALDH1 reactivation. Statistical analysis of quantitative IHC and clinical data showed ALDH1 expression was correlated with higher stage and grade of NSCLC (p = 0.02). Expression of ALDH1 in stage I NSCLC patients was linked to decreased 5 year cancer-specific survival (62% vs. 96%, p = 0.006) and overall survival (32% vs. 72%, p = 0.009). Conclusions: 1. ALDH1 is a NSCLC SC-associated tumor marker. 2. ALDH1 expression is a negative prognostic marker in early stage NSCLC. No significant financial relationships to disclose.
Tspan-1 is a molecular characteristic of ovarian carcinomas
Authors: Claus J. Scholz, Georg Sauer, Jasmin Windisch, Karin Koretz, Rolf Kreienberg, Helmut Deissler
Journal: Clinical Cancer Research (2006)

A115  On the molecular level, cell adhesion, motility and invasiveness are determined by diverse groups of cell surface glycoproteins that influence a wide variety of biological processes by linking cell-cell and cell-matrix interactions to signaling pathways. Among those, tetraspanins play a special role as transmembrane adaptor proteins through the palmitoylation dependent association with each other and a variety of signaling molecules thus creating functional complexes called tetraspanin enriched microdomains or tetraspanin web. For several malignant diseases, e.g. breast, colon, lung, and ovarian cancer, the expression levels of several members of the protein family were found to correlate with the stage of tumor progression or appearance of metastases. Tspan-1 is a yet weakly characterized tetraspanin which, on the basis of expression profiling with cDNA microarrays or differential display techniques, was suggested to contribute substantially to the malignant phenotypes in several human malignancies including pancreatic, cervical and ovarian cancer. The aim of our study is the molecular characterization of Tspan-1, to find its molecular interaction partners and the evaluation whether Tspan-1 expression pattern is a useful marker for the classification of different subtypes of ovarian carcinomas.By immunization of rabbits with synthetic peptides representing parts of the Tspan-1 large extracellular domain, we generated a set of novel anti-Tspan-1 antibodies suitable for Western blot analyses and immunohistochemistry. Western blot analysis of lysates prepared from ovarian carcinoma cell lines revealed that the generated antibodies recognize two specific bands with apparent molecular weights of approximately 26 kDa, which corresponds to the expected molecular weight deduced from the primary structure, and ca. 60 kDa, respectively. His-tag-detected Tspan-1 displays a similar pattern with one additional band, possibly resulting from post-translational modification(s) of the endogenous protein that inhibit antibody binding to the epitope. Expression of Tspan-1 fused to EGFP in several tumor-derived cell lines suggests a subcellular localization of Tspan-1 both in the plasma membrane and intracellular vesicular compartments which include lysosomes as shown by co-localization with LAMP-1. Immunohistochemical analyses of ovarian tumors classified as mucinous (n=10), serous (n=10) and endometrioid (n=10) revealed a strong Tspan-1 expression in tumor epithelium forming pseudoglandular structures. Our results confirm that Tspan-1 contributes to the malignant phenotype of ovarian carcinomas of different types and suggests a role of this tetraspanin in tumor progression. Further analyses of Tspan-19s interactions with other proteins in functional complexes will help to define its role in genesis and growth of ovarian tumors and might provide targets for novel therapeutic approaches.
Systematic Review and Meta-analysis of Diagnostic Accuracy of Percutaneous Renal Tumour Biopsy
Authors: Lorenzo Marconi, Saeed Dabestani, Thomas B. Lam, Fabian Hofmann, Fiona Stewart, John Norrie, Axel Bex, Karim Bensalah, Steven E. Canfield, Milan Hora, Markus A. Kuczyk, Axel S. Merseburger, Peter F.A. Mulders, Thomas Powles, Michael Staehler, Borje Ljungberg, Alessandro Volpe
Journal: European Urology (2015)
Epithelial Dysplasia in Nipple Aspirates of Breast Fluid: Association With Family History and Other Breast Cancer Risk Factors&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;&lt;xref ref-type="fn" rid="FN3"&gt;3&lt;/xref&gt;
Authors: N L Petrakis, V L Ernster, E B King, S T Sacks
Journal: JNCI Journal of the National Cancer Institute (1982)

Because of the strong association of epithelial dysplasia and breast cancer, the extent to which dysplasia of breast fluid epithelial cells obtained by nipple aspiration is associated with breast cancer risk factors was investigated. A significantly higher proportion of women who had a first-degree family history of breast cancer had dysplastic cells in breast fluid than women who had no such history. When family history status was correlated with various breast cancer risk factors, higher proportions of women with dysplasia were found among those who had a first degree family history of breast cancer and for whom certain other risk factors were present, which suggested additive and synergistic effects of these factors on breast epithelium. Breast epithelia of women with a first-degree family history of breast cancer may be more prone to abnormal differentiation in response to environmentally conditioned risk factors.
Molecular mechanisms of nonablative fractionated laser resurfacing
Authors: J.S. Orringer, L. Rittié, D. Baker, J.J. Voorhees, G. Fisher
Journal: British Journal of Dermatology (2010)

Nonablative fractionated laser resurfacing improves the texture of treated skin, but little is known about the molecular mechanisms that underlie clinical improvements.We sought to examine and quantify the time course and magnitude of dermal matrix changes that occur in response to nonablative fractionated laser resurfacing, with the dual goals of better understanding the molecular mechanisms that underlie clinical improvements and of gaining knowledge that will enable evidence-based treatment parameter optimization.Twenty patients (mean age 58 years) with photodamaged skin were focally treated on dorsal forearms with a nonablative fractionated laser. Serial skin samples were obtained at baseline and at various times after treatment. Biopsies were examined with real-time polymerase chain reaction technology and immunohistochemical techniques.Laser treatment resulted in an initial inflammatory response as indicated by statistically significant induction of proinflammatory cytokines (interleukin-1β and tumour necrosis factor-α). This was followed by substantial increases in levels of several matrix metalloproteinases and later by significant induction of type I collagen. Dermal remodelling was noted with both low and high microbeam energy treatment parameters.Nonablative fractionated laser resurfacing induces a well-organized wound-healing response that leads to substantial dermal remodelling and collagen induction. Surprisingly, only minimal differences were observed between lower and higher microbeam energy settings. These data suggest that lower microbeam energy/higher microbeam density treatment parameters, which are generally better tolerated by patients, may yield dermal changes similar to those that result from higher microbeam energy/lower microbeam density treatment parameters.
Serous cystic neoplasm of the pancreas: a multinational study of 2622 patients under the auspices of the International Association of Pancreatology and European Pancreatic Club (European Study Group on Cystic Tumors of the Pancreas)
Authors: B Jais, V Rebours, G Malleo, R Salvia, M Fontana, L Maggino, C Bassi, R Manfredi, R Moran, A M Lennon, A Zaheer, C Wolfgang, R Hruban, G Marchegiani, C Fernández Del Castillo, W Brugge, Y Ha, M H Kim, D Oh, I Hirai, W Kimura, J Y Jang, S W Kim, W Jung, H Kang, S Y Song, C M Kang, W J Lee, S Crippa, M Falconi, I Gomatos, J Neoptolemos, A C Milanetto, C Sperti, C Ricci, R Casadei, M Bissolati, G Balzano, I Frigerio, R Girelli, M Delhaye, B Bernier, H Wang, K T Jang, D H Song, M T Huggett, K W Oppong, L Pererva, K V Kopchak, M Del Chiaro, R Segersvard, L S Lee, D Conwell, A Osvaldt, V Campos, G Aguero Garcete, B Napoleon, I Matsumoto, M Shinzeki, F Bolado, J M Urman Fernandez, M G Keane, S P Pereira, I Araujo Acuna, E C Vaquero, M R Angiolini, A Zerbi, J Tang, R W Leong, A Faccinetto, G Morana, M C Petrone, P G Arcidiacono, J H Moon, H J Choi, R S Gill, D Pavey, M Ouaïssi, B Sastre, M Spandre, C G De Angelis, M A Rios-Vives, M Concepcion-Martin, T Ikeura, K Okazaki, L Frulloni, O Messina, P Lévy
Journal: Gut (2015)

<h3>Objectives</h3> Serous cystic neoplasm (SCN) is a cystic neoplasm of the pancreas whose natural history is poorly known. The purpose of the study was to attempt to describe the natural history of SCN, including the specific mortality. <h3>Design</h3> Retrospective multinational study including SCN diagnosed between 1990 and 2014. <h3>Results</h3> 2622 patients were included. Seventy-four per cent were women, and median age at diagnosis was 58 years (16–99). Patients presented with non-specific abdominal pain (27%), pancreaticobiliary symptoms (9%), diabetes mellitus (5%), other symptoms (4%) and/or were asymptomatic (61%). Fifty-two per cent of patients were operated on during the first year after diagnosis (median size: 40 mm (2–200)), 9% had resection beyond 1 year of follow-up (3 years (1–20), size at diagnosis: 25 mm (4–140)) and 39% had no surgery (3.6 years (1–23), 25.5 mm (1–200)). Surgical indications were (not exclusive) uncertain diagnosis (60%), symptoms (23%), size increase (12%), large size (6%) and adjacent organ compression (5%). In patients followed beyond 1 year (n=1271), size increased in 37% (growth rate: 4 mm/year), was stable in 57% and decreased in 6%. Three serous cystadenocarcinomas were recorded. Postoperative mortality was 0.6% (n=10), and SCN9s related mortality was 0.1% (n=1). <h3>Conclusions</h3> After a 3-year follow-up, clinical relevant symptoms occurred in a very small proportion of patients and size slowly increased in less than half. Surgical treatment should be proposed only for diagnosis remaining uncertain after complete workup, significant and related symptoms or exceptionally when exists concern with malignancy. This study supports an initial conservative management in the majority of patients with SCN. <h3>Trial registration number</h3> IRB 00006477.