tbuckley/cabot-search huggingface dataset:
Interleukin-6 from intrahepatic cells of bone marrow origin is required for normal murine liver regeneration
Authors: Xavier Aldeguer, Fotini Debonera, Abraham Shaked, Alyssa M. Krasinkas, Andrew E. Gelman, Xingyi Que, Gideon A. Zamir, Shungo Hiroyasu, Kellen K. Kovalovich, Rebecca Taub, Kim M. Olthoff
Journal: Hepatology (2002)

Interleukin-6 (IL-6) is required for normal liver regeneration, but the specific cellular source of this growth factor is unknown. We investigated whether this signal originates from the resident macrophage, the Kupffer cell. Using a murine model of bone marrow transplantation, we replaced recipient bone marrow-derived cells, including Kupffer cells, with cells of donor genetic phenotype. Recipients deficient in IL-6 (IL-6 −/− ) were lethally irradiated, then rescued with 10 7 donor bone marrow cells capable of expressing IL-6 (IL-6 +/+ ). Conversely, IL-6 +/+ recipients received IL-6 −/− marrow. Successful engraftment was measured by the presence of the Y chromosome SRY locus in the livers of female recipients receiving male marrow, in situ IL-6 expression by Kupffer cells, and up-regulation of IL-6 in splenocytes after activation with lipopolysaccharide (LPS). Kupffer cell isolation in IL-6 −/− females receiving IL-6 +/+ male marrow clearly showed the presence of the SRY locus and IL-6 disrupted allele, whereas males receiving female marrow demonstrated no SRY or IL-6 signals, confirming the extent of replacement. Replacement of these cells in IL-6 −/− mice with IL-6 +/+ bone marrow successfully restored the regenerative response after partial hepatectomy (PHx) as indicated by signal transduction and activator of transcription 3 (STAT3) activation and hepatocyte DNA replication. Alternatively, complete replacement of Kupffer cells in IL-6 +/+ mice by transplantation with IL-6 −/− cells significantly inhibited liver regeneration and was partially restored by administration of IL-6. This investigation demonstrates a paracrine mechanism by which cells of bone marrow origin, most likely Kupffer cells, regulate the regenerative capacity of the hepatocyte through IL-6 expression.
<i>Squamous Cell Carcinoma Related Oncogene</i>/DCUN1D1 Is Highly Conserved and Activated by Amplification in Squamous Cell Carcinomas
Authors: Inderpal Sarkaria, Pornchai O-charoenrat, Simon G. Talbot, Pabbathi G. Reddy, Ivan Ngai, Ellie Maghami, Kepal N. Patel, Benjamin Lee, Yoshihiro Yonekawa, Maria Dudas, Andrew Kaufman, Russell Ryan, Ronald Ghossein, Pulivarthi H. Rao, Archontoula Stoffel, Y. Ramanathan, Bhuvanesh Singh
Journal: Cancer Research (2006)

Abstract Chromosomal amplification at 3q is common to multiple human cancers, but has a specific predilection for squamous cell carcinomas (SCC) of mucosal origin. We identified and characterized a novel oncogene, SCC-related oncogene (SCCRO), which is amplified along the 3q26.3 region in human SCC. Amplification and overexpression of SCCRO in these tumors correlate with poor clinical outcome. The importance of SCCRO amplification in malignant transformation is established by the apoptotic response to short hairpin RNA against SCCRO, exclusively in cancer cell lines carrying SCCRO amplification. The oncogenic potential of SCCRO is underscored by its ability to transform fibroblasts (NIH-3T3 cells) in vitro and in vivo. We show that SCCRO regulates Gli1—a key regulator of the hedgehog (HH) pathway. Collectively, these data suggest that SCCRO is a novel component of the HH signaling pathway involved in the malignant transformation of squamous cell lineage. (Cancer Res 2006; 66(19): 9437-44)
Hemodynamically important right ventricular infarction: follow-up evaluation of right ventricular systolic function at rest and during exercise with radionuclide ventriculography and respiratory gas exchange.
Authors: L J Dell'Italia, N J Lembo, M R Starling, M H Crawford, R S Simmons, J C Lasher, R Blumhardt, J Lancaster, R A O'Rourke
Journal: Circulation (1987)

The prognosis and recovery of right ventricular systolic function in patients with hemodynamically documented right ventricular myocardial infarction (RVMI) is unclear. Therefore 27 patients who met hemodynamic criteria for RVMI were followed for at least 1 year. Four patients died within 1 year and 23 survived. Postmortem examination performed in three of the four patients showed extensive infarction of the right and left ventricles. Survivors underwent early and late follow-up resting radionuclide ventriculograms and late exercise studies. During long-term follow-up (1 to 4 years) resting radionuclide ventriculography demonstrated a significant improvement in right ventricular ejection fraction (30 +/- 7% to 43 +/- 8%; p less than .001) and right ventricular wall motion index (2.2 +/- 0.4 to 1.5 +/- 0.5; p less than .001) in 18 patients who survived longer than 1 year. Fourteen of these patients underwent upright bicycle exercise while off beta-blocking drugs and peak radionuclide ejection fraction was acquired after anaerobic threshold was achieved. Right ventricular ejection fraction increased significantly from 41 +/- 10% to 47 +/- 12% (p less than .001), as did the left ventricular ejection fraction (55 +/- 15% to 60 +/- 12%; p less than .05). The direction and magnitude of change of the right ventricular ejection fraction correlated significantly with the left ventricular ejection fraction (r = .82, p less than .02). Deviations from this correlation occurred in patients who had a decreased forced expiratory volume in 1 sec and an abnormal ventilatory reserve during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
Diet Therapy for Minority Patients With Diabetes
Authors: Dorothy Gohdes
Journal: Diabetes Care (1988)

The opinions expressed in this paper are those of the author and do not necessarily reflect the views of the Indian Health Service Diet therapy for minority diabetic patients must be directed to NIDDM, the most prominent form of diabetes in minority populations. Diet programs must be tailored to the cultural framework, and traditional foods with desirable characteristics can be encouraged. To teach patients about diet, educators must use educational techniques appropriate to culture and literacy of the patient and family. Single-concept messages such as “eat less fat” or “eat less food” promote learning and minimize failure. Nutrition information can be divided into sequenced manageable steps that can then be individualized to the patient's setting. No single set of exchange lists will suffice for all minority groups, nor are exchange lists themselves appropriate for all situations. To meet the needs of minority patients, nutrition educators must use a variety of tools and techniques relating to the foods of a particular ethnic group. Sound education strategies and simplified materials for NIDDM patients should also be employed.
Direct evidence that the VEGF-specific antibody bevacizumab has antivascular effects in human rectal cancer
Authors: Christopher G Willett, Yves Boucher, Emmanuelle di Tomaso, Dan G Duda, Lance L Munn, Ricky T Tong, Daniel C Chung, Dushyant V Sahani, Sanjeeva P Kalva, Sergey V Kozin, Mari Mino, Kenneth S Cohen, David T Scadden, Alan C Hartford, Alan J Fischman, Jeffrey W Clark, David P Ryan, Andrew X Zhu, Lawrence S Blaszkowsky, Helen X Chen, Paul C Shellito, Gregory Y Lauwers, Rakesh K Jain
Journal: Nature Medicine (2004)
Proceedings: Some new evidence on human joint lubrication.
Authors: A Unsworth, D Dowson, V Wright
Journal: Annals of the Rheumatic Diseases (1973)

After repair of a Bochdalek diaphragmatic hernia, shunting of blood away from the lungs produced progressive hypoxaemia in a neonate. Changes in plasma concentrations of the vasoconstrictor prostanoid thromboxane were associated with changes in pulmonary vascular resistance in this infant. Plasma concentrations of the vasodilator prostanoid prostacyclin were also monitored during acute changes in pulmonary vascular resistance. Tolazoline administration was followed by reductions in pulmonary vascular resistance and in plasma thromboxane and prostacyclin values. Further studies indicated that tolazoline inhibits platelet thromboxane synthesis and vascular prostacyclin synthesis. These data suggest that thromboxane plays a part in the increased pulmonary vascular resistance that occurs after repair of congenital diaphragmatic hernia and that tolazoline may reverse pulmonary hypertension by a mechanism additional to its known action as an alpha adrenergic blocking agent and its effect on histamine release.
Abnormal alveolar macrophage populations in bone marrow transplant recipients with pneumonitis
Authors: HJ Milburn, HG Prentice, LW Poulter
Journal: European Respiratory Journal (1993)

The purpose of this investigation was to determine whether there is any relationship between different subsets of alveolar macrophages and type of infection or survival from interstitial pneumonitis following bone marrow transplantation (BMT). The population of alveolar macrophages found in bronchoalveolar lavage fluid (BALF) from 16 BMT recipients with 19 episodes of interstitial pneumonitis was investigated, using immunocytochemical methods. Results were compared with those from seven normal volunteers. The results showed that patients with pneumonitis had significantly higher numbers of total cells in BALF than normals but reduced proportions of macrophages, although the absolute numbers were unchanged. Of the cells present which were morphologically macrophages, there were raised proportions of both RFD1+ cells (interdigitating cells) and RFD7+ cells (mature macrophages) in patients compared with normals, but expansion of these two subsets could be explained, in part, by a significant increase in cells positive for both markers (42% in patients compared with 9% in normals). Proportions of cells with the monocyte phenotype (CD14+, UCHM1) were also significantly raised in patients with pneumonitis (17% compared with 6% in normals). These patients, however, had significantly reduced proportions of macrophage-like cells which were positive for the DR antigen (Class II major histocompatibility complex (MHC) antigen) (47% compared with 88% in normals), and this abnormality was greater still in patients who died from pneumonitis (40%) compared with those who survived (52%). The results of this study indicate a breakdown of local immunoregulation, thus contributing to the high incidence of, and mortality from, opportunistic pulmonary infections in this group.
First myocardial infarctions in Asian and white men.
Authors: L. O. Hughes, U. Raval, E. B. Raftery
Journal: BMJ (1989)

OBJECTIVE--To compare the presentation and natural course of first myocardial infarctions in immigrant Asians and the indigenous white population in Britain and the subsequent risk states of the two groups. DESIGN--Prospective ethnic comparison of consecutive patients with first myocardial infarctions. SETTING--Secondary referrals to a coronary care unit of a district general hospital. PATIENTS--128 Men (77 white, 54 Asian) presenting consecutively with a first myocardial infarction diagnosed on the basis of clinical, biochemical, and electrocardiographic findings. END POINT--Identification of mechanisms accounting for the increased rate of ischaemic heart disease in Asians. MEASUREMENTS AND MAIN RESULTS--Infarct size was assessed by measuring the release of creatine phosphokinase (all patients), radionuclide ventriculography (50), and contrast ventriculography (103). Risk states after infarction were assessed from the degree of ventricular dysfunction as determined by exercise electrocardiography (82 patients) and from the extent of coronary atheroma as determined by coronary arteriography (103). Glucose state was measured in fasting venous blood samples. Overall the relative rate of infarction was 4.9 times higher in Asians (95% confidence interval 3.4 to 6.9) than in the white population. Moreover, the relative rate of infarction was higher in Asians in all 10 year age groups, the greatest difference being in 30-39 year olds. The mean age of the Asian denominator population was 47.1 years compared with 49.5 years in the white population. Age at infarction was less in Asians (50.2 years) than in white patients (55.5 years; mean difference 5.5 years (95% confidence interval 2.5 to 7.1]. In Asians the mean creatine phosphokinase activity was 777 (95% confidence interval 155 to 1399) U/1 higher, radionuclide ejection fraction 8.9% (1.0% to 16.9%) lower, and left ventricular fractional shortening 4.8% (1.4% to 8.2%) lower than in white patients. The extent of coronary atheroma was significantly greater in Asians. The mean numbers of plaques in vessels not associated with infarction were 3.66 (median 3.0, range 0-10) in Asians compared with 1.97 (median 2.0, range 0-6) in white patients (p less than 0.001), and a higher proportion of Asians had three vessel coronary artery disease (p less than 0.001). Asians with diabetes or impaired glucose tolerance did not differ from those with normal blood glucose values. CONCLUSIONS--Atherogenesis arises earlier in Asians, contributing to premature first myocardial infarctions. The increased incidence of diabetes in Asians may not in itself be relevant in the greater propensity to coronary atheroma in Asians.
Distinct Patterns of Calcium Transients During Early and Delayed Afterdepolarizations Induced by Isoproterenol in Ventricular Myocytes
Authors: Gaetano M. De Ferrari, MariaCristina Viola, Elvira D’Amato, Renzo Antolini, Stefano Forti
Journal: Circulation (1995)

Background The relation between early afterdepolarizations (EADs) and changes in intracellular Ca 2+ concentration ([Ca 2+ ] i ) is still unclear. In the present study, we compared spatiotemporal changes in [Ca 2+ ] i related to EADs and delayed afterdepolarizations (DADs) induced by isoproterenol. Methods and Results Isolated patch-clamped guinea pig ventricular myocytes, loaded with fluo-3 acetoxymethyl ester (fluo-3 AM), were paced at 0.1 to 2 Hz. Isoproterenol (100 nmol/L) caused alterations in both phase 2 and phase 4 of the action potential (AP), consistent with EADs and DADs, respectively. During EADs (n=16), similar to driven APs, increases in [Ca 2+ ] i occurred simultaneously throughout the cell, whereas during DADs (n=25), they originated in discrete cell sites and propagated as a wave. This difference was confirmed by analysis of eight EADs and DADs coupled to the same beat. Ca 2+ transients linked to EADs reached a peak relative fluorescence level (expressed as percentage of the maximal level reached during the last stimulated beat) that was always higher than that reached during the DADs (77±3% versus 64±2%, P &lt;.001). Spatial heterogeneity of Ca 2+ transients was assessed by the maximal time interval between peaks monitored in different cell regions; this time lag was always greater during DADs than during EADs (290 versus 40 milliseconds, P =.006). Conclusions The present study had two main findings. First, even very modest notches occurring during the plateau of the AP may be accompanied by a marked secondary increase in [Ca 2+ ] i . Second, these Ca 2+ transients occurring during EADs are synchronous throughout the cell and differ significantly from those observed under identical conditions during DADs.
Individualised aerobic and resistance exercise training improves cardiorespiratory fitness and reduces cardiovascular risk in patients with rheumatoid arthritis
Authors: Antonios Stavropoulos-Kalinoglou, Giorgos S Metsios, Jet JJCS Veldhuijzen van Zanten, Peter Nightingale, George D Kitas, Yiannis Koutedakis
Journal: Annals of the Rheumatic Diseases (2012)

<h3>Background and objectives</h3> Low cardiorespiratory fitness (CRF) is a significant predictor of cardiovascular disease (CVD), and interventions aiming at increasing CRF are known to reduce CVD risk. The effects of such interventions on CVD risk have not been studied in patients with rheumatoid arthritis (RA). <h3>Methods</h3> 40 age, gender, body mass index (BMI) and disease duration matched RA patients were allocated to either an exercise (receiving 6 months individualised aerobic and resistance high intensity exercise intervention, three times per week), or control (receiving advice on exercise benefits and lifestyle changes) arm. Participants were assessed at baseline, 3 and 6 months for aerobic capacity (VO<sub>2</sub>max), individual CVD risk factors (blood pressure, lipids, insulin resistance, body composition), 10-year CVD event probability and RA characteristics (C-reactive protein (CRP), Disease Activity Score 28 (DAS28) and Health Assessment Questionnaire (HAQ)). <h3>Results</h3> There were no differences between groups at baseline in any of the assessed variables. VO<sub>2</sub>max (p=0.001), blood pressure (systolic: p&lt;0.001; diastolic: p=0.003), triglycerides (p=0.030), high density lipoprotein (HDL; p=0.042), total cholesterol:HDL ratio (p=0.005), BMI (p=0.001), body fat (p=0.026), 10-year CVD event probability (p=0.012), CRP (p=0.042), DAS28 (p=0.008) and HAQ (p=0.003) were all significantly improved in the exercise versus the control group. The change in VO<sub>2</sub>max was the strongest predictor for the observed improvements in all of the assessed CVD risk factors and disease characteristics. <h3>Conclusions</h3> Individualised aerobic and resistance exercise intervention can lead to significantly improved CRF, individual CVD risk factors, composite CVD risk, and disease activity and severity in RA patients.
Radiation-Induced Breast Cancer: Long-Term Follow-up of Radiation Therapy for Benign Breast Disease
Authors: Anders Mattsson, Bengt-Inge Rudén, Per Hall, Nils Wilking, Lars Erik Rutqvist
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article Radiation-Induced Breast Cancer: Long-Term Follow-up of Radiation Therapy for Benign Breast Disease Get access Anders Mattsson, Anders Mattsson Search for other works by this author on: Oxford Academic PubMed Google Scholar Bengt-Inge Rudén, Bengt-Inge Rudén Search for other works by this author on: Oxford Academic PubMed Google Scholar Per Hall, Per Hall Search for other works by this author on: Oxford Academic PubMed Google Scholar Nils Wilking, Nils Wilking Search for other works by this author on: Oxford Academic PubMed Google Scholar Lars Erik Rutqvist Lars Erik Rutqvist Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 20, 20 October 1993, Pages 1679–1685, https://doi.org/10.1093/jnci/85.20.1679 Published: 20 October 1993 Article history Received: 17 February 1993 Revision received: 25 May 1993 Accepted: 19 July 1993 Published: 20 October 1993
Potentiation of endothelium-dependent relaxations to bradykinin by angiotensin I converting enzyme inhibitors in canine coronary artery involves both endothelium-derived relaxing and hyperpolarizing factors.
Authors: J V Mombouli, S Illiano, T Nagao, T Scott-Burden, P M Vanhoutte
Journal: Circulation Research (1992)

Studies were designed to investigate the mechanisms underlying the augmentation by angiotensin I converting enzyme (ACE) inhibitors of the endothelium-dependent relaxations evoked by bradykinin. Isometric tension, tissue levels of cGMP, and transmembrane potential were measured in isolated canine coronary arteries as indications of the respective contribution of nitric oxide and endothelium-derived hyperpolarizing factor. In rings of coronary artery with endothelium, relaxations to bradykinin were potentiated by the ACE inhibitors cilazaprilat and perindoprilat. NG-Nitro-L-arginine (NLA), a nitric oxide synthase inhibitor, impaired relaxations to bradykinin. But the presence of ACE inhibitors partially restored this activity. Bradykinin stimulated the production of cGMP, and this was enhanced significantly by ACE inhibitors, indicating an augmented release of nitric oxide. NLA abolished the increase induced by bradykinin irrespective of the presence of ACE inhibitors. Electrophysiological studies revealed that bradykinin elicited an endothelium-dependent hyperpolarization of vascular smooth muscle that was insensitive to NLA and potentiated by ACE inhibitors. The bradykinin-induced hyperpolarization and NLA-resistant relaxations were transient and impaired by potassium depolarization. Thus, production of endothelium-derived hyperpolarizing factor may account for the NLA-resistant relaxations of canine coronary arteries. The relaxations induced by bradykinin were unaffected by the B1 kinin receptor antagonist des-Arg9,[Leu8]-bradykinin either in the absence or in the presence of NLA but were antagonized by the B2 kinin receptor antagonist D-Arg[Hyp3,D-Phe7]-bradykinin. Molecular exclusion chromatography of 125I-labeled [Tyr8]-bradykinin and its degradation products demonstrated that the breakdown of the kinin by isolated coronary arteries was prevented in the presence of perindoprilat.(ABSTRACT TRUNCATED AT 250 WORDS)
Calcipotriol inhibits rectal epithelial cell proliferation in ulcerative proctocolitis.
Authors: M G Thomas, K P Nugent, A Forbes, R C Williamson
Journal: Gut (1994)

Vitamin D3 reduces human rectal crypt cell production rate (CCPR) and may thereby protect against colorectal cancer. Cell turnover is increased in ulcerative proctocolitis, which might therefore respond to vitamin D3 metabolites. This study investigated the effect of calcipotriol, a synthetic vitamin D3 analogue that avoids hypercalcaemia, on human rectal CCPR in ulcerative proctocolitis. Paired rectal biopsy specimens from seven patients with severe disease were established in organ culture with or without calcipotriol (1 x 10(-6) M). After 15 hours, vincristine (0.6 microgram/ml) was added to induce metaphase arrest, and CCPR was determined by linear regression analysis of accumulated metaphases. Compared with values in 17 controls with incidental anal conditions, median rectal CCPR was 28% higher in ulcerative proctocolitis: 5.90 (5.00-9.50) v 4.80 (2.85-7.07) cells/crypt/hour (p < 0.01). Calcipotriol reduced CCPR by 62% in patients with ulcerative proctocolitis, from 5.90 (5.00-9.50) to 2.21 (0.81-3.22) cells/crypt/hour (median with range) p < 0.01. Thus calcipotriol can dampen the hyperproliferative state in ulcerative proctocolitis and could have a therapeutic role in the control of this inflammatory condition.
Identification of a SIRT1 Mutation in a Family with Type 1 Diabetes
Authors: Anna Biason-Lauber, Marianne Böni-Schnetzler, Basil P. Hubbard, Karim Bouzakri, Andrea Brunner, Claudia Cavelti-Weder, Cornelia Keller, Monika Meyer-Böni, Daniel T. Meier, Caroline Brorsson, Katharina Timper, Gil Leibowitz, Andrea Patrignani, Remy Bruggmann, Gino Boily, Henryk Zulewski, Andreas Geier, Jennifer M. Cermak, Peter Elliott, James L. Ellis, Christoph Westphal, Urs Knobel, Jyrki J. Eloranta, Julie Kerr-Conte, François Pattou, Daniel Konrad, Christian M. Matter, Adriano Fontana, Gerhard Rogler, Ralph Schlapbach, Camille Regairaz, José M. Carballido, Benjamin Glaser, Michael W. McBurney, Flemming Pociot, David A. Sinclair, Marc Y. Donath
Journal: Cell Metabolism (2013)
Family Cancer History: Healthy Skepticism Required
Authors: Rachel A. Freedman, Judy E. Garber
Journal: JNCI Journal of the National Cancer Institute (2011)

cases, diagnoses in family members may also have been missed, either because of difficulty matching cases for which minimal details were available or because cancer registry data were incomplete. Confirmation of true-negative cases is always difficult. It is also unclear how authors resolved conflicts if discrepancies in con firmation were noted or how often this occurred. Other investigators have previously observed more accurate reporting of family history (3–5), although this may be due to the population-based design of the Family Health Study, in which relatively few participants had a personal history of cancer. Cancer patients may be more motivated to understand their family cancer history in greater detail, especially if multiple family members have been affected by a particular diagnosis. In addition, factors such as