tbuckley/cabot-search huggingface dataset:
Diagnosis of gout in patients with asymptomatic hyperuricaemia: a pilot ultrasound study: Table 1
Authors: Eugenio De Miguel, Juan G Puig, Concepción Castillo, Diana Peiteado, Rosa J Torres, Emilio Martín-Mola
Journal: Annals of the Rheumatic Diseases (2011)

<h3>BACKGROUND:</h3> We hypothesized that the lack of benefit of setting a low versus a high PEEP in patients with ARDS may be due in part to differences in the dynamic behavior of the expiratory valve in ventilators. We tested this hypothesis by conducting a bench comparison of the dynamic behavior of expiratory valves on ICU ventilators currently in use. <h3>METHODS:</h3> We attached 7 ICU ventilators (C5, C6, Carescape, PB980, ServoU, V500, and V680) to the ASL 5000 lung model (passive condition with compliance 20 mL/cm H<sub>2</sub>O and resistance 5 cm H<sub>2</sub>O/L/s) and set in volume controlled mode (tidal volume 0.8 L, breathing frequency 10 breaths/min). Flow and pressure were measured just before the exhalation valve. At PEEP of 5, 10, and 15 cm H<sub>2</sub>O, the median instantaneous expiratory resistance, the time to valve opening, and the pressure time products above or below the values of PEEP (expressed in cm H<sub>2</sub>O × s) were determined. <h3>RESULTS:</h3> Median instantaneous expiratory resistance values differed between the ventilators and PEEP settings with a significant interaction: at PEEP 5 cm H<sub>2</sub>O, the median (interquartile range) expiratory resistance values were 3.9 (3.5–4.7), 3.0 (3.0–3.1), 20.9 (15.8–24.9), 27.4 (26.5–43.2), 13.8 (13.6–13.9), 4.4 (4.0–4.6), and 34.3 (33.7–33.8) cm H<sub>2</sub>O/L/s, for the C5, C6, Carescape, PB980, ServoU, V500, and V680, respectively. For all the PEEP settings, the corresponding times to valve opening were 0.080 (0.077–0.082), 0.082 (0.080–0.085), 0.110 (0.105–0.110), 0.100 (0.085–1.05), 0.072 (0.062–0.072), 0.145 (0.115–0.150), and 0.075 (0.070–0.080) s, respectively, and pressure-time products were 2.8 (2.1–7.4), 6.8 (6.7–7.3), 2.4 (2.1–2.4), 3.5 (2.7–3.6), 1.8 (1.8–2.1), 2.8 (2.7–2.9), and 5.7 (5.4–5.9) cm H<sub>2</sub>O × s, respectively. <h3>CONCLUSIONS:</h3> The resistance of active expiratory valves differed significantly between the 7 ICU ventilators tested.
Intrahepatic cholangiographic appearance simulating primary sclerosing cholangitis in several hepatobiliary diseases: A postmortem cholangiographic and histopathological study in 154 livers at autopsy
Authors: Tadashi Terada, Yasuni Nakanuma
Journal: Hepatology (1995)

Intrahepatic cholangiography of primary sclerosing cholangitis (PSC) is characterized by stricture with or without dilation of the biliary tree. To evaluate whether this cholangiographic appearance is present in non-PSC livers as well as the histological features seen in non-PSC livers with this cholangiographic appearance, we performed postmortem intrahepatic cholangiography in 154 liver autopsy specimens. The PSC-like cholangiographic appearance was frequently found in cirrhosis with or without hepatocellular carcinoma (4 of 6, 67%), hepatocellular carcinoma (1 of 1, 100%), adult-type polycystic disease of the liver and kidneys (2 of 3, 67%), submassive hepatic necrosis (2 of 5, 40%), amyloidosis (1 of 2, 50%), and intrahepatic extensive thrombosis (1 of 1, 100%). It was also found but at lower frequency in metastatic carcinomas (3 of 13, 23%) and leukemia/lymphoma infiltration (2 of 12, 17%). Histologically, in livers with such a PSC-like cholangiographic appearance, the intrahepatic bile ducts were compressed by fibrosis, inflammatory infiltrates, liver cysts, cancer cell infiltration, amyloid deposition, or portal thrombi. Dilated ducts had less pronounced changes than strictured ducts. In these hepatobiliary diseases, the changes of intrahepatic bile ducts in the livers without the PSC-like cholangiographic appearance were much less marked than those in the livers with it. These data suggest that the PSC-like intrahepatic cholangiographic appearance is present in several hepatobiliary diseases and that clinicians should take such diseases into consideration if stricture with or without dilation is found on intrahepatic cholangiography.
Comparative Analyses of Chromosome Alterations in Soft-Tissue Metastases within and across Patients with Castration-Resistant Prostate Cancer
Authors: Ilona N. Holcomb, Janet M. Young, Ilsa M. Coleman, Keyan Salari, Douglas I. Grove, Li Hsu, Lawrence D. True, Martine P. Roudier, Colm M. Morrissey, Celestia S. Higano, Peter S. Nelson, Robert L. Vessella, Barbara J. Trask
Journal: Cancer Research (2009)

Abstract Androgen deprivation is the mainstay of therapy for progressive prostate cancer. Despite initial and dramatic tumor inhibition, most men eventually fail therapy and die of metastatic castration-resistant (CR) disease. Here, we characterize the profound degree of genomic alteration found in CR tumors using array comparative genomic hybridization (array CGH), gene expression arrays, and fluorescence in situ hybridization (FISH). Bycluster analysis, we show that the similarity of the genomic profiles from primary and metastatic tumors is driven by the patient. Using data adjusted for this similarity, we identify numerous high-frequency alterations in the CR tumors, such as 8p loss and chromosome 7 and 8q gain. By integrating array CGH and expression array data, we reveal genes whose correlated values suggest they are relevant to prostate cancer biology. We find alterations that are significantly associated with the metastases of specific organ sites, and others with CR tumors versus the tumors of patients with localized prostate cancer not treated with androgen deprivation. Within the high-frequency sites of loss in CR metastases, we find an overrepresentation of genes involved in cellular lipid metabolism, including PTEN. Finally, using FISH, we verify the presence of a gene fusion between TMPRSS2 and ERG suggested by chromosome 21 deletions detected by array CGH. We find the fusion in 54% of our CR tumors, and 81% of the fusion-positive tumors contain cells with multiple copies of the fusion. Our investigation lays the foundation for a better understanding of and possible therapeutic targets for CR disease, the poorly responsive and final stage of prostate cancer. [Cancer Res 2009;69(19):7793–802]
Vesnarinone Restores Contractility and Calcium Handling in Early Endotoxemia
Authors: K. Takeuchi, P. J. del Nido, D. N. Poutias, D. B. Cowan, M. Munakata, F. X. McGowan
Journal: Circulation (2000)

Endotoxin (lipopolysaccharide, LPS) is a trigger of the systemic inflammatory response. We have previously found that vesnarinone and amrinone, when given before LPS, prevented cytokine production and LPS-related cardiac dysfunction. We tested the hypothesis that vesnarinone would improve intracellular Ca(2+) handling and calcium-activated contractile force after the onset of endotoxemia.Adult rabbits received a bolus injection of LPS or vehicle. Vesnarinone (3 mg/kg) was given intravenously 90 minutes later. Two hours after LPS administration, hearts were perfused in the isolated Langendorff mode. Peak left ventricular developed pressure, +/-dp/dt, oxygen consumption (MVO(2)), and ratexpressure product were evaluated in conjunction with fluorescent spectroscopic determinations of intracellular calcium concentrations (Ca(i)) and the rate of Ca(i) transient decline during diastole (tauCa). Peak left ventricular developed pressure and +/-dp/dt were significantly lower in the LPS group. These were completely restored by vesnarinone. There was significantly slower diastolic calcium removal (increased tauCa) in LPS hearts that was also corrected by vesnarinone; however, the cytosolic calcium overload characteristic of LPS hearts was only partially improved. Reduced mechanical inefficiency (the ratio of rate-pressure product to MVO(2)) and myofilament sensitivity to Ca(i) were also significantly improved by vesnarinone.Acute endotoxemia caused contractile protein calcium insensitivity, oxygen wastage, and abnormal calcium cycling. Vesnarinone, given in the rescue mode, normalized LPS-induced myocardial dysfunction and partially restored abnormal calcium cycling. Although the mechanisms responsible for these effects require further clarification, it appears that agents such as vesnarinone may be useful to treat inflammatory-induced myocardial dysfunction.
The contributions of normal variation and genetic background to mammalian gene expression
Authors: Colin Pritchard, David Coil, Sarah Hawley, Li Hsu, Peter S Nelson
Journal: Genome biology (2006)

Abstract Background Qualitative and quantitative variability in gene expression represents the substrate for external conditions to exert selective pressures for natural selection. Current technologies allow for some forms of genetic variation, such as DNA mutations and polymorphisms, to be determined accurately on a comprehensive scale. Other components of variability, such as stochastic events in cellular transcriptional and translational processes, are less well characterized. Although potentially important, the relative contributions of genomic versus epigenetic and stochastic factors to variation in gene expression have not been quantified in mammalian species. Results In this study we compared microarray-based measures of hepatic transcript abundance levels within and between five different strains of Mus musculus . Within each strain 23% to 44% of all genes exhibited statistically significant differences in expression between genetically identical individuals (positive false discovery rate of 10%). Genes functionally associated with cell growth, cytokine activity, amine metabolism, and ubiquitination were enriched in this group. Genetic divergence between individuals of different strains also contributed to transcript abundance level differences, but to a lesser extent than intra-strain variation, with approximately 3% of all genes exhibiting inter-strain expression differences. Conclusion These results indicate that although DNA sequence fixes boundaries for gene expression variability, there remain considerable latitudes of expression within these genome-defined limits that have the potential to influence phenotypes. The extent of normal or expected natural variability in gene expression may provide an additional level of phenotypic opportunity for natural selection.
Regulation of the renal Na-HCO3 cotransporter
Authors: O S Ruiz, Y Y Qiu, L J Wang, J A Arruda
Journal: Journal of the American Society of Nephrology (1995)

Angiotensin II stimulates proximal tubule acidification by activating both the Na-H antiporter and the Na-HCO3 cotransporter. The mechanism whereby angiotensin II stimulates the Na-HCO3 cotransporter was investigated in renal cortical basolateral membrane vesicles of the rabbit by measuring 22Na uptake in the presence of HCO3 and gluconate. Na-HCO3 cotransporter activity (expressed in nanomoles per milligram of protein per 3 s) was taken as the difference in 22Na uptake in the presence of HCO3 and gluconate. Angiotensin II stimulated Na-HCO3 cotransporter activity significantly (control, 1.5 +/- 0.4; angiotensin II, 3.3 +/- 0.6; P < 0.05), and this stimulation was prevented by the angiotensin II receptor antagonist DuP 753. Angiotensin II has been shown to stimulate both pertussis toxin-sensitive Gi protein and pertussis toxin-insensitive Gq protein. In the presence of pertussis toxin, angiotensin II (10(-11) M) failed to stimulate the Na-HCO3 cotransporter, suggesting a role of Gi protein in mediating this effect. In the presence of a polyclonal antibody against Gi protein, angiotensin II failed to stimulate the Na-HCO3 cotransporter (control, 1.6 +/- 0.4; angiotensin II, 3.9 +/- 0.9; angiotensin II + Gi, 1.2 +/- 0.7). Angiotensin II stimulated inositol triphosphate release, and this effect could be blocked by the phospholipase C inhibitor U73122, suggesting a role of phospholipase C or A2 in this effect of angiotensin II. In the presence of the protein kinase C inhibitor calphostin C (50 nM), angiotensin II also failed to stimulate the Na-HCO3 cotransporter. These results demonstrate that angiotensin II stimulates the renal Na-HCO3 cotransporter by interacting with a specific angiotensin II receptor and that this stimulation is mediated by the activation of Gi and Gq proteins.
Passive transfer of diabetes from BB/W to Wistar-Furth rats.
Authors: S B Koevary, D E Williams, R M Williams, W L Chick
Journal: Journal of Clinical Investigation (1985)

Autoimmune diabetes can be transferred to young, diabetes prone BB/W rats by injecting them intravenously with concanavalin A (Con A)-treated spleen cells from acute diabetic BB/W donors. This study describes the transfer of diabetes to the normal Wistar-Furth strain of rats using a similar procedure. For the successful transfer of diabetes it was necessary to immunosuppress recipient animals with a single intraperitoneal injection of cyclophosphamide 24-48 h before administering Con A-stimulated spleen cells from acute diabetic BB/W rats. Of 68 Wistar-Furth rats in immunosuppressed with a dose of 100-150 mg cyclophosphamide/kg body wt, 10 (15%) became diabetic. None of the control rats receiving either Con A-stimulated Wistar-Furth spleen cells (n = 28), freshly isolated BB/W spleen cells (n = 14), or fresh RPMI medium (n = 11) became diabetic. These data indicate that diabetes can be transferred from BB/W to Wistar-Furth rats. In addition, they support the hypothesis that cell-mediated immune processes are involved in the development of insulin-dependent diabetes and rule out any absolute requirement for BB-derived genes in the target pancreatic beta cells.
Sequestration of Plasmodium falciparum–infected erythrocytes to chondroitin sulfate A, a receptor for maternal malaria: monoclonal antibodies against the native parasite ligand reveal pan-reactive epitopes in placental isolates
Authors: Jean-Bernard Lekana Douki, Boubacar Traore, Fabio T. M. Costa, Thierry Fusaı̈, Bruno Pouvelle, Yvon Sterkers, Artur Scherf, Jürg Gysin
Journal: Blood (2002)
CCL2-dependent infiltrating macrophages promote angiogenesis in progressive liver fibrosis
Authors: Josef Ehling, Matthias Bartneck, Xiao Wei, Felix Gremse, Viktor Fech, Diana Möckel, Christer Baeck, Kanishka Hittatiya, Dirk Eulberg, Tom Luedde, Fabian Kiessling, Christian Trautwein, Twan Lammers, Frank Tacke
Journal: Gut (2014)

<h3>Objectives</h3> In chronic liver injury, angiogenesis, the formation of new blood vessels from pre-existing ones, may contribute to progressive hepatic fibrosis and to development of hepatocellular carcinoma. Although hypoxia-induced expression of vascular endothelial growth factor (VEGF) occurs in advanced fibrosis, we hypothesised that inflammation may endorse hepatic angiogenesis already at early stages of fibrosis. <h3>Design</h3> Angiogenesis in livers of c57BL/6 mice upon carbon tetrachloride- or bile duct ligation-induced chronic hepatic injury was non-invasively monitored using in vivo contrast-enhanced micro computed tomography (µCT) and ex vivo anatomical µCT after hepatic Microfil perfusion. Functional contributions of monocyte-derived macrophage subsets for angiogenesis were explored by pharmacological inhibition of CCL2 using the Spiegelmer mNOX-E36. <h3>Results</h3> Contrast-enhanced in vivo µCT imaging allowed non-invasive monitoring of the close correlation of angiogenesis, reflected by functional hepatic blood vessel expansion, with experimental fibrosis progression. On a cellular level, inflammatory monocyte-derived macrophages massively accumulated in injured livers, colocalised with newly formed vessels in portal tracts and exhibited pro-angiogenic gene profiles including upregulated VEGF and MMP9. Functional in vivo and anatomical ex vivo µCT analyses demonstrated that inhibition of monocyte infiltration by targeting the chemokine CCL2 prevented fibrosis-associated angiogenesis, but not fibrosis progression. Monocyte-derived macrophages primarily fostered sprouting angiogenesis within the portal vein tract. Portal vein diameter as a measure of portal hypertension depended on fibrosis, but not on angiogenesis. <h3>Conclusions</h3> Inflammation-associated angiogenesis is promoted by CCL2-dependent monocytes during fibrosis progression. Innovative in vivo µCT methodology can accurately monitor angiogenesis and antiangiogenic therapy effects in experimental liver fibrosis.
Electroanatomic Remodeling of the Left Stellate Ganglion After Myocardial Infarction
Authors: Seongwook Han, Kenzaburo Kobayashi, Boyoung Joung, Gianfranco Piccirillo, Mitsunori Maruyama, Harry V. Vinters, Keith March, Shien-Fong Lin, Changyu Shen, Michael C. Fishbein, Peng-Sheng Chen, Lan S. Chen
Journal: Journal of the American College of Cardiology (2012)
Breast cancer cells stimulate osteoprotegerin (OPG) production by endothelial cells through direct cell contact
Authors: Penny E Reid, Nicola J Brown, Ingunn Holen
Journal: Molecular Cancer (2009)

Abstract Background Angiogenesis, the sprouting of capillaries from existing blood vessels, is central to tumour growth and progression, however the molecular regulation of this process remains to be fully elucidated. The secreted glycoprotein osteoprotegerin (OPG) is one potential pro-angiogenic factor, and clinical studies have demonstrated endothelial cells within a number of tumour types to express high levels of OPG compared to those in normal tissue. Additionally, OPG can increase endothelial cell survival, proliferation and migration, as well as induce endothelial cell tube formation in vitro . This study aims to elucidate the processes involved in the pro-angiogenic effects of OPG in vitro , and also how OPG levels may be regulated within the tumour microenvironment. Results It has previously been demonstrated that OPG can induce tube formation on growth factor reduced matrigel. In this study, we demonstrate that OPG enhances the pro-angiogenic effects of VEGF and that OPG does not stimulate endothelial cell tube formation through activation of the VEGFR2 receptor. We also show that cell contact between HuDMECs and the T47D breast cancer cell line increases endothelial cell OPG mRNA and protein secretion levels in in vitro co-cultures. These increases in endothelial cell OPG secretion were dependent on α ν β 3 ligation and NFκB activation. In contrast, the pro-angiogenic factors VEGF, bFGF and TGFβ had no effect on HuDMEC OPG levels. Conclusion These findings suggest that the VEGF signalling pathway is not involved in mediating the pro-angiogenic effects of OPG on endothelial cells in vitro . Additionally, we show that breast cancer cells cause increased levels of OPG expression by endothelial cells, and that direct contact between endothelial cells and tumour cells is required in order to increase endothelial OPG expression and secretion. Stimulation of OPG secretion was shown to involve α ν β 3 ligation and NFκB activation.
Computed Tomographic Measurement of Airway Remodeling and Emphysema in Advanced Chronic Obstructive Pulmonary Disease. Correlation with Pulmonary Hypertension
Authors: Gaël Dournes, François Laurent, Florence Coste, Claire Dromer, Elodie Blanchard, François Picard, Fabien Baldacci, Michel Montaudon, Pierre-Olivier Girodet, Roger Marthan, Patrick Berger
Journal: American Journal of Respiratory and Critical Care Medicine (2014)

Rationale: Pulmonary hypertension (PH) is an established complication of advanced chronic obstructive pulmonary disease (COPD) associated with increased mortality. The mechanisms coupling PH and bronchial obstruction are unknown; in particular, PH appears to be unrelated to emphysema. We hypothesized that computed tomographic (CT) measurement of airway remodeling instead of emphysema may correlate with PH in COPD.Objectives: We aimed to describe the clinical and CT characteristics of patients with COPD with or without PH and to correlate CT measurements of airway remodeling and emphysema with PH.Methods: Data were retrieved from 60 COPD patients who underwent both right heart catheterization and computed tomography in a period of stability and had no other disease known to cause PH. CT measurement of airway wall thickness (WT-Pi10) was used to assess airway remodeling and low lung area percentage (LAA%) to quantify emphysema extent.Measurements and Main Results: Thirty-four of the sixty patients with COPD had PH (mean pulmonary arterial pressure [PAPm] ≥ 25 mm Hg). There was no difference between the two groups regarding age, sex, and spirometric results, whereas there was more profound hypoxemia in the PH group. WT-Pi10 was increased in the patients with COPD and PH and correlated with PAPm (ρ = 0.62; P < 0.001). Conversely, there was no difference or correlation between PAPm and LAA% (ρ = 0.12; P = 0.33). In multivariate analysis (R2 = 0.53), WT-Pi10 was the independent predictor most associated with PAPm elevation, as compared to hypoxia (PaO2) or pulmonary arterial enlargement (diameter ratio between the pulmonary arterial truncus and the ascending aorta).Conclusions: This study demonstrates, for the first time to our knowledge, an association between structural alterations of bronchi and PH in COPD. Unlike quantification of emphysema, CT measurement of airway remodeling correlates with PAPm and could be used to estimate the severity of PH in COPD. Airway remodeling burden is not limited to airflow limitation in the assessment of COPD severity and mortality.
Altered Functional Magnetic Resonance Imaging Responses to Nonpainful Sensory Stimulation in Fibromyalgia Patients
Authors: Marina López‐Solà, Jesus Pujol, Tor D. Wager, Alba Garcia‐Fontanals, Laura Blanco‐Hinojo, Susana Garcia‐Blanco, Violant Poca‐Dias, Ben J. Harrison, Oren Contreras‐Rodríguez, Jordi Monfort, Ferran Garcia‐Fructuoso, Joan Deus
Journal: Arthritis & Rheumatology (2014)

Fibromyalgia (FM) is a disorder characterized by chronic pain and enhanced responses to acute noxious events. However, the sensory systems affected in FM may extend beyond pain itself, as FM patients show reduced tolerance to non-nociceptive sensory stimulation. Characterizing the neural substrates of multisensory hypersensitivity in FM may thus provide important clues about the underlying pathophysiology of the disorder. The aim of this study was to characterize brain responses to non-nociceptive sensory stimulation in FM patients and their relationship to subjective sensory sensitivity and clinical pain severity.Functional magnetic resonance imaging (MRI) was used to assess brain response to auditory, visual, and tactile motor stimulation in 35 women with FM and 25 matched controls. Correlation and mediation analyses were performed to establish the relationship between brain responses and 3 types of outcomes: subjective hypersensitivity to daily sensory stimulation, spontaneous pain, and functional disability.Patients reported increased subjective sensitivity (increased unpleasantness) in response to multisensory stimulation in daily life. Functional MRI revealed that patients showed reduced task-evoked activation in primary/secondary visual and auditory areas and augmented responses in the insula and anterior lingual gyrus. Reduced responses in visual and auditory areas were correlated with subjective sensory hypersensitivity and clinical severity measures.FM patients showed strong attenuation of brain responses to nonpainful events in early sensory cortices, accompanied by an amplified response at later stages of sensory integration in the insula. These abnormalities are associated with core FM symptoms, suggesting that they may be part of the pathophysiology of the disease.