tbuckley/cabot-search huggingface dataset:
Tuberculosis screening in migrants in selected European countries shows wide disparities
Authors: R. Coker
Journal: European Respiratory Journal (2006)

Well-established tuberculosis screening units in Western Europe were selectively sampled. Three screening units in Norway, two in the UK, one in the Netherlands and one in Switzerland were evaluated. The aim of this study was to describe a range of service models used at a number of individual tuberculosis units for the screening of new entrants into Europe. Semi-structured interviews were conducted with clinicians, nurses and administrators from a selected sample of European tuberculosis screening units. An outline of key themes to be addressed was forwarded to units ahead of scheduled interviews. Themes included the history of the unit, structure, processes and outputs involved in screening new entrants for tuberculosis. Considerable variation in screening services exists in the approaches studied. Units are sited in transit camps or as units within hospital facilities. Staff capacity and administration varies from one clinic per week with few dedicated staff to fully dedicated units. Only one site recorded symptoms; tuberculin testing was universal in children, but varied in adults; chest radiograph screening was universal except at one site where a positive tuberculin skin test or symptoms were required in those &lt;35 yrs of age before ordering a radiograph. Few output data are routinely and systematically collected, which hinders comparison and determination of effectiveness and efficiency. Service models for screening new immigrants for tuberculosis appear to vary in Western Europe. The systematic collection of data would make international comparisons between units easier and help draw conclusions that might usefully inform service development.
Aurora Kinase A Promotes Ovarian Tumorigenesis through Dysregulation of the Cell Cycle and Suppression of BRCA2
Authors: Gong Yang, Bin Chang, Fan Yang, Xiaoqing Guo, Kathy Qi Cai, Xue (Sherry) Xiao, Huamin Wang, Subrata Sen, Mien-Chie Hung, Gordon B. Mills, Sandy Chang, Asha S. Multani, Imelda Mercado-Uribe, Jinsong Liu
Journal: Clinical Cancer Research (2010)

Abstract Purpose: Aurora kinase A (Aurora-A) is known to regulate genomic instability and tumorigenesis in multiple human cancers. The underlying mechanism, however, is not fully understood. We examined the molecular mechanism of Aurora-A regulation in human ovarian cancer. Experimental Design: Retrovirus-mediated small hairpin RNA (shRNA) was used to silence the expression of Aurora-A in the ovarian cancer cell lines SKOV3, OVCA432, and OVCA433. Immunofluorescence, Western blotting, flow cytometry, cytogenetic analysis, and animal assay were used to test centrosome amplification, cell cycle alteration, apoptosis, DNA damage response, tumor growth, and genomic instability. Immunostaining of BRCA2 and Aurora-A was done in ovarian, pancreatic, breast, and colon cancer samples. Results: Knockdown of Aurora-A reduced centrosome amplification, malformation of mitotic spindles, and chromosome aberration, leading to decreased tumor growth. Silencing Aurora-A attenuated cell cycle progression and enhanced apoptosis and DNA damage response by restoring p21, pRb, and BRCA2 expression. Aurora-A was inversely correlated with BRCA2 in high-grade ovarian serous carcinoma, breast cancer, and pancreatic cancer. In high-grade ovarian serous carcinoma, positive expression of BRCA2 predicted increased overall and disease-free survival, whereas positive expression of Aurora-A predicted poor overall and disease-free survival (P &amp;lt; 0.05). Moreover, an increased Aurora-A to BRCA2 expression ratio predicted poor overall survival (P = 0.047) compared with a decreased Aurora-A to BRCA2 expression ratio. Conclusion: Aurora-A regulates genomic instability and tumorigenesis through cell cycle dysregulation and BRCA2 suppression. The negative correlation between Aurora-A and BRCA2 exists in multiple cancers, whereas the expression ratio of Aurora-A to BRCA2 predicts ovarian cancer patient outcome. Clin Cancer Res; 16(12); 3171–81. ©2010 AACR.
Risk of Vascular Access Complications with Frequent Hemodialysis
Authors: Rita S. Suri, Brett Larive, Susan Sherer, Paul Eggers, Jennifer Gassman, Sam H. James, Robert M. Lindsay, Robert S. Lockridge, Daniel B. Ornt, Michael V. Rocco, George O. Ting, Alan S. Kliger
Journal: Journal of the American Society of Nephrology (2013)

Frequent hemodialysis requires using the vascular access more often than with conventional hemodialysis, but whether this increases the risk for access-related complications is unknown. In two separate trials, we randomly assigned 245 patients to receive in-center daily hemodialysis (6 days per week) or conventional hemodialysis (3 days per week) and 87 patients to receive home nocturnal hemodialysis (6 nights per week) or conventional hemodialysis, for 12 months. The primary vascular access outcome was time to first access event (repair, loss, or access-related hospitalization). Secondary outcomes were time to all repairs and time to all losses. In the Daily Trial, 77 (31%) of 245 patients had a primary outcome event: 33 repairs and 15 losses in the daily group and 17 repairs, 11 losses, and 1 hospitalization in the conventional group. Overall, the risk for a first access event was 76% higher with daily hemodialysis than with conventional hemodialysis (hazard ratio [HR], 1.76; 95% confidence interval [CI], 1.11–2.79; P=0.017); among the 198 patients with an arteriovenous (AV) access at randomization, the risk was 90% higher with daily hemodialysis (HR, 1.90; 95% CI, 1.11–3.25; P=0.02). Daily hemodialysis patients had significantly more total AV access repairs than conventional hemodialysis patients (P=0.011), with 55% of all repairs involving thrombectomy or surgical revision. Losses of AV access did not differ between groups (P=0.58). We observed similar trends in the Nocturnal Trial, although the results were not statistically significant. In conclusion, frequent hemodialysis increases the risk of vascular access complications. The nature of the AV access repairs suggests that this risk likely results from increased hemodialysis frequency rather than heightened surveillance.
Presinusoidal and proximal intrasinusoidal confluence of hepatic artery and portal vein in rat liver: Functional evidence by orthograde and retrograde bivascular perfusion
Authors: Yuji Watanabe, Gerhard P. Püschel, Andreas Gardemann, Kurt Jungermann
Journal: Hepatology (1994)

The site of confluence of the artery and the portal vein in the liver still appears to be controversial. Anatomical studies suggested a presinusoidal or an intrasinusoidal confluence in the first, second or even final third of the sinusoids. The objective of this investigation was to study the problem with functional biochemical techniques. Rat livers were perfused through the hepatic artery and simultaneously either in the orthograde direction from the portal vein to the hepatic vein or in the retrograde direction from the hepatic vein to the portal vein. Arterial flow was linearly dependent on arterial pressure between 70 cm H2O and 120 cm H2O at a constant portal or hepatovenous pressure of 18 cm H2O. An arterial pressure of 100 cm H2O was required for the maintenance of a homogeneous orthograde perfusion of the whole parenchyma and of a physiologic ratio of arterial to portal flow of about 1:3. Glucagon was infused either through the artery or the portal vein and hepatic vein, respectively, to a submaximally effective "calculated" sinusoidal concentration after mixing of 0.1 nmol/L. During orthograde perfusions, arterial and portal glucagon caused the same increases in glucose output. Yet during retrograde perfusions, hepatovenous glucagon elicited metabolic alterations equal to those in orthograde perfusions, whereas arterial glucagon effected changes strongly reduced to between 10% and 50%. Arterially infused trypan blue was distributed homogeneously in the parenchyma during orthograde perfusions, whereas it reached clearly smaller areas of parenchyma during retrograde perfusions. Finally, arterially applied acridine orange was taken up by all periportal hepatocytes in the proximal half of the acinus during orthograde perfusions but only by a much smaller portion of periportal cells in the proximal third of the acinus during retrograde perfusions. These findings suggest that in rat liver, the hepatic artery and the portal vein mix before and within the first third of the sinusoids, rather than in the middle or even last third.
The Role of Particulate Matter-Associated Zinc in Cardiac Injury in Rats
Authors: Urmila P. Kodavanti, Mette C. Schladweiler, Peter S. Gilmour, J. Grace Wallenborn, Bhaskar S. Mandavilli, Allen D. Ledbetter, David C. Christiani, Marschall S. Runge, Edward D. Karoly, Daniel L. Costa, Shyamal Peddada, Richard Jaskot, Judy H. Richards, Ronald Thomas, Nageswara R. Madamanchi, Abraham Nyska
Journal: Environmental Health Perspectives (2007)

Exposure to particulate matter (PM) has been associated with increased cardiovascular morbidity; however, causative components are unknown. Zinc is a major element detected at high levels in urban air.We investigated the role of PM-associated zinc in cardiac injury.We repeatedly exposed 12- to 14-week-old male Wistar Kyoto rats intratracheally (1x/week for 8 or 16 weeks) to a) saline (control); b) PM having no soluble zinc (Mount St. Helens ash, MSH); or c) whole-combustion PM suspension containing 14.5 microg/mg of water-soluble zinc at high dose (PM-HD) and d ) low dose (PM-LD), e) the aqueous fraction of this suspension (14.5 microg/mg of soluble zinc) (PM-L), or f ) zinc sulfate (rats exposed for 8 weeks received double the concentration of all PM components of rats exposed for 16 weeks).Pulmonary inflammation was apparent in all exposure groups when compared with saline (8 weeks > 16 weeks). PM with or without zinc, or with zinc alone caused small increases in focal subepicardial inflammation, degeneration, and fibrosis. Lesions were not detected in controls at 8 weeks but were noted at 16 weeks. We analyzed mitochondrial DNA damage using quantitative polymerase chain reaction and found that all groups except MSH caused varying degrees of damage relative to control. Total cardiac aconitase activity was inhibited in rats receiving soluble zinc. Expression array analysis of heart tissue revealed modest changes in mRNA for genes involved in signaling, ion channels function, oxidative stress, mitochondrial fatty acid metabolism, and cell cycle regulation in zinc but not in MSH-exposed rats.These results suggest that water-soluble PM-associated zinc may be one of the causal components involved in PM cardiac effects.
FURACIN SOLUBLE DRESSING IN THE TREATMENT OF VARICOSE ULCERS
Authors: JAMES SOMMERVILLE, DENIS C. DEVINE
Journal: British Journal of Dermatology (1952)

Journal Article FURACIN SOLUBLE DRESSING IN THE TREATMENT OF VARICOSE ULCERS Get access JAMES SOMMERVILLE, M. B., F. R. F. P. S.(G.), JAMES SOMMERVILLE, M. B., F. R. F. P. S.(G.) Senior Consultant Dermatologist, Dermatological Department, Western Infirmary Group, Glasgow Search for other works by this author on: Oxford Academic Google Scholar DENIS C. DEVINE, M. D. DENIS C. DEVINE, M. D. Senior Hospital Medical Officer, Dermatological Department, Western Infirmary Group, Glasgow Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 64, Issue 10, 1 October 1952, Pages 361–365, https://doi.org/10.1111/j.1365-2133.1952.tb15798.x Published: 01 October 1952
Pericardial Pressure during Transverse Acceleration in Dogs without Thoracotomy
Authors: NATALIO BANCHERO, WILHELM J. RUTISHAUSER, ANASTASIOS G. TSAKIRIS, EARL H. WOOD
Journal: Circulation Research (1967)

Intrapericardial pressures were recorded via a saline-filled Teflon catheter (o. d., 1.3 mm) in 11 anesthetized dogs studied without thoracotomy. Seven animals were studied before, during, and after 1-min exposures to transverse accelerations that ranged from 1G (normal gravitational environment) to 7G when in the supine (+G j ), prone (-G x ), left decubitus (+G v ), and right decubitus (-G y ) positions. Four additional animals were studied at 1G only, while in these same body positions. Pressures also were recorded from both atria, right ventricle, aorta, esophagus, and the potential pleural space. Mean end-expiratory intrapericardial pressure varied directly with the vertical height of the recording site in the thorax during all conditions studied, as would be expected in a hydrostatic system. Transpericardial pressures were not significantly different from zero at all levels of acceleration studied. Transmural left and right atrial pressures were independent of the height of the recording site in the thorax and were unchanged during exposures to transverse accelerations that ranged from plus to minus 7G x .
Modulation of intestinal and systemic immune responses to a fed protein antigen, in mice.
Authors: S Strobel, A Ferguson
Journal: Gut (1986)

Feeding of a protein antigen to normal adult mice results in systemic immunologic hyporesponsiveness (oral tolerance). Local mucosal cell mediated immunity is not usually elicited. The objectives of these experiments were to abrogate the induction of oral tolerance and concomitantly to induce a local mucosal cell mediated immune response in mice; and thereby to establish which facets of intestinal physiology or immunology are relevant to the induction of normal, mainly suppressor immune responses to a fed antigen. Protein antigen (ovalbumin) was fed to animals in whom immune status had been modulated by intraperitoneal injection of N-acetyl-muramyl dipeptide (MDP), by induction of a graft versus host reaction, or naturally, by virtue of immaturity. The induction of oral tolerance was prevented in all treatment groups. In a second series of experiments mice were orally immunised as before, rested for four weeks, and then challenged with ovalbumin in their drinking water for 10 days. Jejunal architecture was not altered by the antigen challenge, but MDP treated and immature animals which had been sensitised to ovalbumin and later re-exposed to the same antigen had significantly higher intraepithelial lymphocyte counts than appropriate controls. Factors which may lead to abrogation of oral tolerance and induction of intestinal hypersensitivity are discussed in relation to food allergic diseases in man.
Effects of chronic ethanol feeding on serum lipoprotein metabolism in the rat
Authors: Enrique Baraona, Charles S. Lieber
Journal: Journal of Clinical Investigation (1970)

In rats, chronic ethanol feeding was found to enhance the postprandial hyperlipemia and to increase the incorporation of dietary palmitic acid-(3)H and intravenously injected L-lysine-(14)C into serum lipoproteins. The main increases of total amount, labeling, and specific activity of lipid and protein occurred in the d < 1.019 lipoprotein fraction. Fat absorption and the clearance of injected chylomicrons were not affected by ethanol feeding. Blocking of lipoprotein and chylomicron removal with Triton did not prevent the action of ethanol on serum lipids, indicating that the ethanol effect is not likely due to defective removal of lipids from the circulation. Ethanol enhanced the incorporation of chylomicron fatty acids into newly synthetized very low density lipoproteins, as shown by an increased reappearance of the fatty acid label into the lipids of this fraction after injection of palmitate-(14)C/glycerol-(3)H doubly labeled chylomicrons. These results indicate that alcoholic hyperlipemia is due, at least in part, to an increase in newly synthetized lipoproteins. The hyperlipemia produced by ethanol was accompanied by hepatic steatosis. The simultaneous production of fatty liver and hyperlipemia makes it unlikely that defective lipoprotein synthesis or secretion is a primary mechanism for the pathogenesis of the alcoholic fatty liver.
Influence of the renin-angiotensin system on the effect of prostaglandin synthesis inhibitors in the renal vasculature.
Authors: S Satoh, B G Zimmerman
Journal: Circulation Research (1975)

The effect of meclofenamate and indomethacin on renal blood flow and renal vascular resistance was determined under basal experimental conditions and during renal ischemia in pentobarbital-anesthetized dogs. Renal blood flow was measured with an electromagnetic flowmeter and renal arterial pressure was recorded from a catheter in the renal artery. Intra-arterial infusion of indomethacin or meclofenamate in concentrations of 4 and 4 to 8 mu-g/ml, respectively, did not cause any significant change in renal blood flow or renal vascular resistance under basal conditions. During the period of ischemia (50% reduction in renal blood flow), 4 mu-g/ml of either prostaglandin synthetase inhibitor caused a marked increase in renal vascular resistance. Prostaglandin E in the renal venous blood was decreased at the time renal vascular resistance was increased by meclofenamate. The renal vasoconstrictor response to angiotensin II injected intravenously was potentiated by both inhibitors under basal as well as ischemic conditions, which also suggested that prostaglandin synthesis was inhibited. The angiotensin antagonist 1-sar-8-ala-angiotensin II was infused intra-arterially in concentrations of 20 and 40 mmu-g/ml during renal ischemia. Subsequent administration of meclofenamate increased renal vascular resistance only slightly. The results of these experiments indicated that renal prostaglandins have more influence on renal blood flow during renal ischemia than under basal conditions, and that the renin-angiotensin system may be involved in activating synthesis and release of prostaglandins during ischemia.
Methicillin-Resistant<i>Staphylococcus aureus</i>
Authors: Franklin D. Lowy
Journal: JAMA Internal Medicine (2013)

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Antisense to Thyrotropin Releasing Hormone Receptor Reduces Arterial Blood Pressure in Spontaneously Hypertensive Rats
Authors: Satoshi Suzuki, Paul Pilowsky, Jane Minson, Leonard Arnolda, Ida Llewellyn-Smith, John Chalmers
Journal: Circulation Research (1995)

Abstract We report in the present study the effect of intrathecal treatment with antisense oligonucleotides complementary to thyrotropin releasing hormone (TRH) receptor mRNA on the pressor response to intrathecal administration of TRH and on resting arterial blood pressure in Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). In 16-week-old male WKY rats, 18-base phosphodiester antisense or mismatch oligonucleotides to TRH receptor mRNA (100 μg per day) were injected intrathecally for 3 days. Twenty-four hours after the last injection, the magnitude of the pressor response to intrathecal TRH (10 μg) was significantly smaller in the antisense-treated group (n=7) compared with mismatch-treated controls (n=7) (change in mean arterial pressure, +20.3±3.0 versus +32.6±2.5 mm Hg, P &lt;.01). No differences were observed in the pressor responses to injection of N -methyl- d -aspartic acid. Resting arterial blood pressure was unaffected by antisense treatment in WKY rats. In separate experiments, 16-week-old male SHR were treated with antisense (n=7) or mismatch (n=6) oligonucleotides for 3 days. Mean resting arterial blood pressure was significantly reduced by treatment with antisense oligonucleotides (from 157±4.8 to 119±8.8 mm Hg, P &lt;.01), but no significant changes were observed in mismatch-treated animals. Our results suggest that the expression of TRH receptors in spinal sympathetic preganglionic neurons can be selectively reduced by intrathecal treatment with antisense oligonucleotides and that TRH projections to sympathetic preganglionic neurons play an important role in the elevation of arterial blood pressure in SHR.
Historical Lessons in Translational Medicine
Authors: Desmond J. Fitzgerald, Garret A. FitzGerald
Journal: Circulation Research (2013)

The development of drugs that inhibit platelets has been driven by a combination of clinical insights, fundamental science, and sheer luck. The process has evolved as the days of stumbling on therapeutic gems, such as aspirin, have long passed and have been replaced by an arduous process in which a drug is designed to target a specific protein implicated in a well-characterized pathophysiological process, or so we would like to believe. The development of antiplatelet therapy illustrates the importance of understanding the mechanisms of disease and the pharmacology of the compounds we develop, coupled with careful clinical experimentation and observation and, yes, still, a fair bit of luck.
A Comprehensive Survey of Ras Mutations in Cancer
Authors: Ian A. Prior, Paul D. Lewis, Carla Mattos
Journal: Cancer Research (2012)

Abstract All mammalian cells express 3 closely related Ras proteins, termed H-Ras, K-Ras, and N-Ras, that promote oncogenesis when they are mutationally activated at codon 12, 13, or 61. Although there is a high degree of similarity among the isoforms, K-Ras mutations are far more frequently observed in cancer, and each isoform displays preferential coupling to particular cancer types. We examined the mutational spectra of Ras isoforms curated from large-scale tumor profiling and found that each isoform exhibits surprisingly distinctive codon mutation and amino-acid substitution biases. These findings were unexpected given that these mutations occur in regions that share 100% amino-acid sequence identity among the 3 isoforms. Of importance, many of these mutational biases were not due to differences in exposure to mutagens, because the patterns were still evident when compared within specific cancer types. We discuss potential genetic and epigenetic mechanisms, as well as isoform-specific differences in protein structure and signaling, that may promote these distinct mutation patterns and differential coupling to specific cancers. Cancer Res; 72(10); 2457–67. ©2012 AACR.
Clinical aspects of blastomycosis
Authors: R. P. O'Neill, R. W. Penman
Journal: Thorax (1970)

Blastomycosis is a specific granulomatous disease which tends to be chronic and indolent. It frequently presents in extrapulmonary form by means of haematogenous dissemination from the lungs. It has been shown that tuberculosis, histoplasmosis and coccidioidomycosis are, in the majority of cases, mild and subclinical in effect and often heal without therapy. It is probable that blastomycosis behaves in a like manner. The exact mortality is not known but is probably in the range of 13% in hospitalized cases with disseminated disease (Blastomycosis Cooperative Study of the Veterans Administration, 1964). The most effective form of therapy in active disease is amphotericin B; 2-hydroxy-stilbamidine is also used. Blastomycosis has largely been considered to be a disease of the American continent. However, cases have been reported from Africa and Europe and therefore a wider appreciation of this disease is considered pertinent. The relevant literature has been reviewed and four illustrative cases are presented.