tbuckley/cabot-search huggingface dataset:
Transatrial Access to the Normal Pericardial Space
Authors: Richard L. Verrier, Sergio Waxman, Eric G. Lovett, Ricardo Moreno
Journal: Circulation (1998)

Background —A nonsurgical means to access the normal pericardial space could provide opportunities for diagnostic sampling and therapeutic interventions. Because there are currently no approved nonsurgical methods to accomplish this, we tested a new approach in large animals. Methods and Results —A catheter system was employed in a percutaneous approach from a femoral vein to pierce the right atrial appendage. Pericardial access was confirmed by placement of a radiopaque guidewire visible under fluoroscopy (6 dogs, 13 pigs). In 7 of the pigs, pericardial tamponade, produced by injection of saline or heparinized blood into the pericardial space through this route, was confirmed by fluoroscopy and hemodynamic evidence. The feasibility and safety of this access route were tested with multiple repetitions in all 19 animals. At the end of each of the 17 acute experiments, direct inspection after thoracotomy revealed no hemopericardium, laceration, or bleeding on catheter withdrawal. In 24-hour survival studies performed in 2 of the 6 dogs, the animals exhibited no behavioral signs of discomfort or untoward consequences on recovery from anesthesia. Histology revealed only a small (≈1-mm) fibrinous plug at the site of puncture. Conclusions —The percutaneous approach via the right atrial appendage provides a rapid, safe route to access the normal pericardial space for diagnostic sampling and to alleviate high-volume and low-volume (&lt;200 mL) pericardial effusions. The access route is potentially useful for selective administration of therapeutic agents, growth factors, gene vectors, and cardioactive and vasoactive agents to the heart.
Identification of functional PGH2/TxA2 receptors on human endothelial cells.
Authors: K C Kent, L J Collins, F T Schwerin, M K Raychowdhury, J A Ware
Journal: Circulation Research (1993)

Although functional receptors for thromboxane A2 and prostaglandin H2 (TxA2/PGH2) have been identified in platelets and vascular smooth muscle cells, receptor-mediated events in human endothelial cells stimulated by these endoperoxides have not been shown. Using cultured endothelial cells harvested from human umbilical or saphenous veins, we measured the effect of the TxA2 mimetic U46619 on mobilization of cytoplasmic calcium ([Ca2+]i), as well as release of prostacyclin and expression of the proto-oncogene c-fos, intracellular events that have been linked to [Ca2+]i rise in stimulated endothelial cells. Addition of U46619 to confluent fura 2-loaded endothelial cells caused a concentration-dependent rise in intracellular [Ca2+]i, with agonist concentrations of 300 nM producing a maximal [Ca2+]i rise. This [Ca2+]i rise was a uniform response observed in all individual endothelial cells throughout the monolayer, as shown by microspectrofluorimetric visualization. Similar effects were seen with a structurally dissimilar endoperoxide analogue, I-BOP, and with the naturally occurring endoperoxide PGH2. The initial [Ca2+]i rise was not reduced when extracellular [Ca2+]i was chelated with EGTA, but a later "plateau" phase was eliminated. An antagonist of the receptor for TxA2/PGH2 (SQ29548) strongly inhibited [Ca2+]i mobilization. Stimulation of endothelial cells with U46619 also transiently increased expression of the proto-oncogene c-fos, as determined by RNA hybridization, and induced a fivefold increase in prostacyclin release. Thus, endoperoxides can stimulate human venous endothelial cells by means of TxA2/PGH2 receptors, whose occupancy can activate intracellular events associated with functional changes.
Differences in risk factors, atherosclerosis, and cardiovascular disease between ethnic groups in Canada: the Study of Health Assessment and Risk in Ethnic groups (SHARE)
Authors: Sonia S Anand, Salim Yusuf, Vladmir Vuksan, Sudarshan Devanesen, Koon K Teo, Patricia A Montague, Linda Kelemen, Cheelong Yi, Eva Lonn, Hertzel Gerstein, Robert A Hegele, Matthew McQueen
Journal: The Lancet (2000)
The long noncoding RNA SPRY4-IT1 increases the proliferation of human breast cancer cells by upregulating ZNF703 expression
Authors: Yongguo Shi, Juan Li, Yangchen Liu, Jie Ding, Yingrui Fan, Yun Tian, Li Wang, Yifan Lian, Keming Wang, Yongqian Shu
Journal: Molecular Cancer (2015)

Long noncoding RNAs (lncRNAs) have emerged recently as a new class of genes that regulate cellular processes, such as cell growth and apoptosis. The SPRY4 intronic transcript 1 (SPRY4-IT1) is a 708-bp lncRNA on chromosome 5 with a potential functional role in tumorigenesis. The clinical significance of SPRY4-IT1 and the effect of SPRY4-IT1 on cancer progression are unclear.Quantitative reverse transcriptase PCR (qRT-PCR) was performed to investigate the expression of SPRY4-IT1 in 48 breast cancer tissues and four breast cancer cell lines. Gain and loss of function approaches were used to investigate the biological role of SPRY4-IT1 in vitro. Microarray bioinformatics analysis was performed to identify the putative targets of SPRY4-IT1, which were further verified by rescue experiments, and by western blotting and qRT-PCR.SPRY4-IT1 expression was significantly upregulated in 48 breast cancer tumor tissues comparedwith normal tissues. Additionally, increased SPRY4-IT1 expression was found to be associated with a larger tumor size and an advanced pathological stage in breast cancer patients. The knockdown of SPRY4-IT1 significantly suppressed proliferation and caused apoptosis of breast cancer cells in vitro. Furthermore, we discovered that ZNF703 was a target of SPRY4-IT1 and was downregulated by SPRY4-IT1 knockdown. Moreover, we provide the first demonstration that ZNF703 plays an oncogenic role in ER (-) breast carcinoma cells.SPRY4-IT1 is a novel prognostic biomarker and a potential therapeutic candidate for breast cancer.
Diagnosing occupational asthma: use of induced sputum
Authors: C Lemiere, MM Pizzichini, R Balkissoon, L Clelland, A Efthimiadis, D O'Shaughnessy, J Dolovich, FE Hargreave
Journal: European Respiratory Journal (1999)

The diagnosis of occupational asthma (OA) needs to be made with as much objective evidence as possible. If there is airway inflammation, measurement of this should be an asset. The objective of this study was to investigate whether there is an increase in induced sputum and blood eosinophils and eosinophil cationic protein (ECP) in OA after work exposure. Patients were assessed after a 2-4 week period at work and away from work with cell counts and ECP assays performed blind to the clinical data. They were considered to have OA if symptoms were worse at work and there was a fall in forced expiratory volume in one second (FEV1) &gt; or =20% or in the provocative concentration of methacholine causing a 20% fall in FEV1 (PC20) of four-fold or more compared with away from work. Patients whose symptoms were worse at work but had a change in FEV1 of &lt;20% and in methacholine PC20 of less than four-fold were considered as controls. Sixteen patients were studied. Ten had OA and six were controls. Patients with OA had a significant increase in median (interquartile range) sputum eosinophils and ECP when at work compared with the periods out of work, 10.0 (17.05) versus 0.8 (1.6)% (p=0.007) and 3,840 (6,076) versus 116 (180) microg x L(-1) (p=0.01). They also had a higher blood eosinophil count, 0.3 (0.5) x 10(9) versus 0.2 (0.1) x 10(9) x L(-1) (p=0.013), and a trend towards higher serum ECP levels, 44.0 (20.0) versus 32.0 (18.5) microg x L(-1) (p=0.07). In conclusion, the proportion of eosinophils and levels of eosinophil cationic protein in sputum are particularly high at work in patients with occupational asthma, suggesting that the measurement of these factors can supplement other physiological outcomes in establishing the diagnosis of occupational asthma.
Argon plasma coagulation for flexible endoscopic Zenker’s diverticulotomy
Authors: T. Rabenstein, A. May, J. Michel, H. Manner, O. Pech, L. Gossner, C. Ell
Journal: Endoscopy (2007)

See also: Commentaire de "Traitement endoscopique du diverticule de Zenker: le choix des armes", pp. 141, 131, 137, 146Endoscopy 2007; 39(02): 193-193DOI: 10.1055/s-0032-1306914
Molecular Mechanisms of Chronic Kidney Transplant Rejection via Large-Scale Proteogenomic Analysis of Tissue Biopsies
Authors: Aleksey Nakorchevsky, Johannes A. Hewel, Sunil M. Kurian, Tony S. Mondala, Daniel Campbell, Steve R. Head, Christopher L. Marsh, John R. Yates, Daniel R. Salomon
Journal: Journal of the American Society of Nephrology (2010)

The most common cause of kidney transplant failure is the poorly characterized histopathologic entity interstitial fibrosis and tubular atrophy (IFTA). There are no known unifying mechanisms, no effective therapy, and no proven preventive strategies. Possible mechanisms include chronic immune rejection, inflammation, drug toxicity, and chronic kidney injury from secondary factors. To gain further mechanistic insight, we conducted a large-scale proteogenomic study of kidney transplant biopsies with IFTA of varying severity. We acquired proteomic data using tandem mass spectrometry with subsequent quantification, analysis of differential protein expression, validation, and functional annotations to known molecular networks. We performed genome-wide expression profiling in parallel. More than 1400 proteins with unique expression profiles traced the progression from normal transplant biopsies to biopsies with mild to moderate and severe disease. Multiple sets of proteins were mapped to different functional pathways, many increasing with histologic severity, including immune responses, inflammatory cell activation, and apoptosis consistent with the chronic rejection hypothesis. Two examples include the extensive population of the alternative rather than the classical complement pathway, previously not appreciated for IFTA, and a comprehensive control network for the actin cytoskeleton and cell signaling of the acute-phase response. In summary, this proteomic effort using kidney tissue contributes mechanistic insight into several biologic processes associated with IFTA.
A Model of Directional Selection Applied to the Evolution of Drug Resistance in HIV-1
Authors: C. Seoighe, F. Ketwaroo, V. Pillay, K. Scheffler, N. Wood, R. Duffet, M. Zvelebil, N. Martinson, J. McIntyre, L. Morris, W. Hide
Journal: Molecular Biology and Evolution (2007)

Understanding how pathogens acquire resistance to drugs is important for the design of treatment strategies, particularly for rapidly evolving viruses such as HIV-1. Drug treatment can exert strong selective pressures and sites within targeted genes that confer resistance frequently evolve far more rapidly than the neutral rate. Rapid evolution at sites that confer resistance to drugs can be used to help elucidate the mechanisms of evolution of drug resistance and to discover or corroborate novel resistance mutations. We have implemented standard maximum likelihood methods that are used to detect diversifying selection and adapted them for use with serially sampled reverse transcriptase (RT) coding sequences isolated from a group of 300 HIV-1 subtype C–infected women before and after single-dose nevirapine (sdNVP) to prevent mother-to-child transmission. We have also extended the standard models of codon evolution for application to the detection of directional selection. Through simulation, we show that the directional selection model can provide a substantial improvement in sensitivity over models of diversifying selection. Five of the sites within the RT gene that are known to harbor mutations that confer resistance to nevirapine (NVP) strongly supported the directional selection model. There was no evidence that other mutations that are known to confer NVP resistance were selected in this cohort. The directional selection model, applied to serially sampled sequences, also had more power than the diversifying selection model to detect selection resulting from factors other than drug resistance. Because inference of selection from serial samples is unlikely to be adversely affected by recombination, the methods we describe may have general applicability to the analysis of positive selection affecting recombining coding sequences when serially sampled data are available.
STUDIES ON THE EXTRACELLULAR CULTIVATION OF AN INTRACELLULAR PARASITE (AVIAN MALARIA)
Authors: William Trager
Journal: The Journal of Experimental Medicine (1952)

The extracellular survival and development in vitro of the erythrocytic stages of Plasmodium lophurae were favored by the addition to the culture medium of l-malic acid and concentrates rich in coenzyme A. In a concentrated extract of duck erythrocytes supplemented with these two substances in addition to adenosinetriphosphate, sodium pyruvate, and certain other materials of like nature, only 5 to 10 per cent of the extracellular parasites had become abnormal after 3 days of cultivation.
Tumor Stage Affects Risk and Prognosis of Contralateral Breast Cancer: Results From a Large Swedish-Population–Based Study
Authors: Voralak Vichapat, Hans Garmo, Marit Holmqvist, Göran Liljegren, Fredrik Wärnberg, Mats Lambe, Tommy Fornander, Jan Adolfsson, Margreet Lüchtenborg, Lars Holmberg
Journal: Journal of Clinical Oncology (2012)

Purpose The number of breast cancer survivors at risk of developing contralateral breast cancer (CBC) is increasing. However, ambiguity remains regarding risk factors and prognosis for women with CBC. Patients and Methods In a cohort of 42,670 women with breast cancer in the Uppsala/Örebro and Stockholm regions in Sweden in 1992 to 2008, we assessed risk factors for and prognosis of metachronous CBC by using survival analysis. Breast cancer–specific survival for women with CBC was evaluated and compared with results for women with unilateral breast cancer (UBC) by using time-dependent Cox-regression modeling. Results An increased risk for CBC was observed among women who had primary breast cancer with ≥ 10 involved lymph nodes compared with node-negative women (adjusted hazard ratio [HR], 1.8; 95% CI, 1.2 to 2.7). The prognosis was poorer in women with CBC than with UBC. The hazard of dying from breast cancer was especially high for women with a short interval time to CBC (adjusted HR, 2.3; 95% CI, 1.8 to 2.8 for CBC diagnosed ≤ 5 years v UBC) and gradually decreased with longer follow-up time but remained higher than the hazard originating from the primary tumor for ≥ 10 years. Conclusion Women with advanced-stage primary breast cancer had an increased risk of developing CBC. CBC is associated with an increased risk of dying from breast cancer throughout a long period of follow-up after the primary tumor. Our findings suggest that the event of CBC marks a new clinical situation in terms of investigations for metastases, treatment considerations, and follow-up strategy.
Enhanced production of monocyte chemotactic protein 3 in inflammatory bowel disease mucosa
Authors: J Wedemeyer, A Lorentz, M Göke, P N Meier, P Flemming, C A Dahinden, M P Manns, S C Bischoff
Journal: Gut (1999)

BACKGROUND The β chemokine monocyte chemotactic protein 3 (MCP-3) has chemoattractant and activating capabilities in monocytes, lymphocytes, eosinophils, and basophils. AIMS To investigate MCP-3 expression in inflammatory conditions of the human intestinal mucosa. PATIENTS Forty five colon biopsy specimens from 18 patients with inflammatory bowel disease (IBD; 16 specimens from inflamed and 10 from non-inflamed areas) and 19 control patients were examined. METHODS Immunohistochemical staining and reverse transcription polymerase chain reaction (RT-PCR) were used for MCP-3 detection in tissue sections. Intestinal epithelial cell lines (HT-29, Caco-2, T-84) were stimulated with interleukin (IL) 1β, IL-6, and tumour necrosis factor α (TNF-α) and examined for MCP-3 protein and mRNA expression using immunocytochemistry and RT-PCR, respectively. RESULTS In tissue sections, MCP-3 protein was detected predominantly in epithelial cells, both in patients with IBD and in controls. MCP-3 staining was particularly pronounced at sites of active mucosal inflammation. The intensity of MCP-3 staining was positively correlated with the extent of epithelial destruction. In intestinal epithelial cell lines, MCP-3 mRNA was expressed, whereas MCP-3 protein was not consistently detected. CONCLUSIONS Our data show that MCP-3 protein is present in normal and inflamed intestinal tissue. MCP-3 production is substantially enhanced in areas of active inflammation, suggesting an immunoregulatory role of MCP-3 in intestinal inflammation.
Genome-wide association study identifies multiple risk loci for chronic lymphocytic leukemia
Authors: Sonja I Berndt, Christine F Skibola, Vijai Joseph, Nicola J Camp, Alexandra Nieters, Zhaoming Wang, Wendy Cozen, Alain Monnereau, Sophia S Wang, Rachel S Kelly, Qing Lan, Lauren R Teras, Nilanjan Chatterjee, Charles C Chung, Meredith Yeager, Angela R Brooks-Wilson, Patricia Hartge, Mark P Purdue, Brenda M Birmann, Bruce K Armstrong, Pierluigi Cocco, Yawei Zhang, Gianluca Severi, Anne Zeleniuch-Jacquotte, Charles Lawrence, Laurie Burdette, Jeffrey Yuenger, Amy Hutchinson, Kevin B Jacobs, Timothy G Call, Tait D Shanafelt, Anne J Novak, Neil E Kay, Mark Liebow, Alice H Wang, Karin E Smedby, Hans-Olov Adami, Mads Melbye, Bengt Glimelius, Ellen T Chang, Martha Glenn, Karen Curtin, Lisa A Cannon-Albright, Brandt Jones, W Ryan Diver, Brian K Link, George J Weiner, Lucia Conde, Paige M Bracci, Jacques Riby, Elizabeth A Holly, Martyn T Smith, Rebecca D Jackson, Lesley F Tinker, Yolanda Benavente, Nikolaus Becker, Paolo Boffetta, Paul Brennan, Lenka Foretova, Marc Maynadie, James McKay, Anthony Staines, Kari G Rabe, Sara J Achenbach, Celine M Vachon, Lynn R Goldin, Sara S Strom, Mark C Lanasa, Logan G Spector, Jose F Leis, Julie M Cunningham, J Brice Weinberg, Vicki A Morrison, Neil E Caporaso, Aaron D Norman, Martha S Linet, Anneclaire J De Roos, Lindsay M Morton, Richard K Severson, Elio Riboli, Paolo Vineis, Rudolph Kaaks, Dimitrios Trichopoulos, Giovanna Masala, Elisabete Weiderpass, María-Dolores Chirlaque, Roel C H Vermeulen, Ruth C Travis, Graham G Giles, Demetrius Albanes, Jarmo Virtamo, Stephanie Weinstein, Jacqueline Clavel, Tongzhang Zheng, Theodore R Holford, Kenneth Offit, Andrew Zelenetz, Robert J Klein, John J Spinelli, Kimberly A Bertrand, Francine Laden, Edward Giovannucci, Peter Kraft, Anne Kricker, Jenny Turner, Claire M Vajdic, Maria Grazia Ennas, Giovanni M Ferri, Lucia Miligi, Liming Liang, Joshua Sampson, Simon Crouch, Ju-Hyun Park, Kari E North, Angela Cox, John A Snowden, Josh Wright, Angel Carracedo, Carlos Lopez-Otin, Silvia Bea, Itziar Salaverria, David Martin-Garcia, Elias Campo, Joseph F Fraumeni, Silvia de Sanjose, Henrik Hjalgrim, James R Cerhan, Stephen J Chanock, Nathaniel Rothman, Susan L Slager
Journal: Nature Genetics (2013)
Effects of Bile Acids on Carcinogen-Exposed Rat Colon in Organ Culture and as Subsequent Long-Term Transplants2
Authors: Betti Reiss, Carol J. Weiss, Takuji Tanaka, Bandaru Reddy, Gary M. Williams
Journal: JNCI Journal of the National Cancer Institute (1987)

Rat (F344) colon fragments in organ culture were exposed for 4 to 6 hours to carcinogens and then for 4 days to deoxycholic acid or fecal extracts containing a mixture of in vivo-produced bile acids from animals fed low- or high-fat diets. Following exposures during culture, the fragments were transplanted into the mammary fat pads of syngeneic rats. The transplanted fragments survived for at least 1 year with preservation of crypt architecture and with continued DNA and mucin synthesis. Exposure in culture to N-methyl-N′-nitro-N-nitrosoguanidine (CAS: 70-25-7) or N-methyl-N-nitrosourea (CAS: 684-93-5) resulted in hypercellularity, hyperplasia, and cellular atypia in the transplants; but, in contrast to transplants from colon adenocarcinomas, no tumors formed. Exposure in culture to deoxycholic acid subsequent to N-methyl-N-nitrosourea or N-methyl-N′-nitro-N-nitrosoguanidine resulted in greater cellular abnormalities in transplants. Exposure after N-methyl-N-nitrosourea to fecal extracts from rats on a high-fat diet also enhanced the pathologic changes, whereas similar extracts from rats on a low-fat diet did not alter the pathology resulting from N-methyl-N-nitrosourea or N-methyl-N′-nitro-N-nitrosoguanidine exposures. It is concluded that bile acids, including those formed in vivo, facilitate the expression of carcinogen-induced abnormalities in the colon mucosa.
Economic Appraisal of Ontario's Universal Influenza Immunization Program: A Cost-Utility Analysis
Authors: Beate Sander, Jeffrey C. Kwong, Chris T. Bauch, Andreas Maetzel, Allison McGeer, Janet M. Raboud, Murray Krahn
Journal: PLoS Medicine (2010)

In July 2000, the province of Ontario, Canada, initiated a universal influenza immunization program (UIIP) to provide free seasonal influenza vaccines for the entire population. This is the first large-scale program of its kind worldwide. The objective of this study was to conduct an economic appraisal of Ontario's UIIP compared to a targeted influenza immunization program (TIIP).A cost-utility analysis using Ontario health administrative data was performed. The study was informed by a companion ecological study comparing physician visits, emergency department visits, hospitalizations, and deaths between 1997 and 2004 in Ontario and nine other Canadian provinces offering targeted immunization programs. The relative change estimates from pre-2000 to post-2000 as observed in other provinces were applied to pre-UIIP Ontario event rates to calculate the expected number of events had Ontario continued to offer targeted immunization. Main outcome measures were quality-adjusted life years (QALYs), costs in 2006 Canadian dollars, and incremental cost-utility ratios (incremental cost per QALY gained). Program and other costs were drawn from Ontario sources. Utility weights were obtained from the literature. The incremental cost of the program per QALY gained was calculated from the health care payer perspective. Ontario's UIIP costs approximately twice as much as a targeted program but reduces influenza cases by 61% and mortality by 28%, saving an estimated 1,134 QALYs per season overall. Reducing influenza cases decreases health care services cost by 52%. Most cost savings can be attributed to hospitalizations avoided. The incremental cost-effectiveness ratio is Can$10,797/QALY gained. Results are most sensitive to immunization cost and number of deaths averted.Universal immunization against seasonal influenza was estimated to be an economically attractive intervention.