tbuckley/cabot-search huggingface dataset:
Gait patterns in COPD: the Rotterdam Study
Authors: Lies Lahousse, Vincentius J.A. Verlinden, Jos N. van der Geest, Guy F. Joos, Albert Hofman, Bruno H.C. Stricker, Guy G. Brusselle, M. Arfan Ikram
Journal: European Respiratory Journal (2015)

Gait disturbances in patients with chronic obstructive pulmonary disease (COPD) may lead to disability and falls. As studies assessing gait kinematics in COPD are sparse, we investigated associations of COPD with various gait domains and explored a potential link with falling. Gait was measured within the prospective, population-based Rotterdam Study (age ≥55 years) using an electronic walkway and summarised into seven gait domains: Rhythm, Variability, Phases, Pace, Tandem, Turning and Base of Support. Rhythm is a temporal gait aspect that includes cadence and reflects how quickly steps are taken. Persons with COPD (n=196) exhibited worse Rhythm (−0.21 sd , 95% CI −0.36– −0.06 sd ) compared with persons with normal lung function (n=898), independent of age, sex, height, education, smoking or analgesic use, especially when dyspnoea and severe airflow limitation or frequent exacerbations (Global Initiative for Chronic Obstructive Lung Disease group D: −0.83 sd , 95% CI −1.25– −0.41 sd ) were present. A lower forced expiratory volume in 1 s was associated with worse Rhythm and Pace, including lower cadence and gait velocity, respectively. Importantly, fallers with COPD had significantly worse Rhythm than nonfallers with COPD. This study demonstrates that persons with COPD exhibit worse Rhythm, especially fallers with COPD. The degree of Rhythm deterioration was associated with the degree of airflow limitation, symptoms and frequency of exacerbations.
Comparison of different equations to assess glomerular filtration in critically ill patients
Authors: Mieke Carlier, Alexander Dumoulin, Alexander Janssen, Sven Picavet, Steve Vanthuyne, Ria Van Eynde, Raymond Vanholder, Joris Delanghe, Gert De Schoenmakere, Jan J. De Waele, Eric A. J. Hoste
Journal: Intensive Care Medicine (2015)
Randomised, double-blind, placebo-controlled clinical trial of a new topical glyceryl trinitrate patch for chronic lateral epicondylosis: Table 1
Authors: J A Paoloni, G A C Murrell, R M Burch, R Y Ang
Journal: British Journal of Sports Medicine (2008)

Objective: This study aimed to determine whether a new glyceryl trinitrate patch preparation is effective in treating chronic lateral epicondylosis. Design: Randomised double-blind controlled clinical trial. Setting: Private practice patients: 154 adult patients with chronic lateral epicondylosis were recruited, with 136 patients completing the trial. Interventions: 8 weeks of glyceryl trinitrate patch application (dosages of 72 mg/24 h, 1.44 mg/24 h, and 3.6 mg/24 h), or placebo patch application. Main outcome measures: Subjective global assessment of change in elbow symptoms, patient-rated tennis elbow evaluation, visual analogue pain at rest, visual analogue pain with activity, visual analogue pain intensity, grip strength, and strength testing using the Orthopaedic Research Institute-Tennis Elbow Testing System. Results: At 8 weeks there was a significant decrease in elbow pain with activity in the glyceryl trinitrate 0.72 mg/24 h group compared with placebo (p = 0.04). There were no other significant differences. Conclusions: Continuous 1.25 mg/24 h topical glyceryl trinitrate treatment, when combined with daily exercise rehabilitation, has previously demonstrated efficacy in treating chronic lateral epicondylosis. There was significantly decreased elbow pain with activity at 8 weeks in the glyceryl trinitrate 0.72 mg/24 h group (p = 0.04). This short-term dose-ranging study did not demonstrate a treatment effect of a new topical glyceryl trinitrate patch in dosages of 1.44 mg/24 h or 3.6 mg/24 h, which conflicts with previous studies on topical glyceryl trinitrate treatment. Trial registration number: NCT00447928.
Paracrine up-regulation of monocyte cyclooxygenase-2 by platelets: Role of transforming growth factor-β1
Authors: S ELIGINI, S BARBIERI, I ARENAZ, E TREMOLI, S COLLI
Journal: Cardiovascular Research (2006)

To examine the role of platelets and platelet-derived products on cyclooxygenase-2 (Cox-2) induction in adherent monocytes and to address the signaling pathways involved.Platelets and monocytes were obtained from peripheral blood of healthy donors. Adherent monocytes were co-cultured with autologous platelets or platelet releasates or exposed to mediators contained in platelet alpha-granules (either from platelet source or recombinant) for 4-24 h. Cox-2 protein and mRNA were determined by Western and RT-PCR analysis, respectively. Thromboxane B2 (TxB2) and prostaglandin E2 (PGE2) synthesis as index of Cox-2 activity, and levels of transforming growth factor-beta1 (TGF-beta1) in platelet releasates were measured by enzyme immunoassay (EIA).Activated platelets induce rapid and transient Cox-2 de novo synthesis in adherent monocytes. The effect is dependent upon the platelet number but not upon cell-cell contact. Platelet-induced Cox-2 was not affected by prevention of platelet TxA2 synthesis or microparticle formation but was blunted by inhibition of platelet alpha-granule secretion. TGF-beta1, either platelet-derived or recombinant (rTGF-beta1), induced Cox-2 expression and activity in adherent monocytes at concentrations within the range of those detected in releasates from activated platelets; this effect was not shared by recombinant platelet-derived growth factor (rPDGFBB). The time course of Cox-2 induction by TGF-beta1 in monocytes was identical to that observed with platelet releasates. Moreover, TGF-beta1 receptor blockade completely abolished platelet-induced Cox-2 expression. p38 MAPK activation represents a common transduction pathway through which activated platelets and rTGF-beta1 induce Cox-2 in monocytes.These findings suggest that TGF-beta1 released by activated platelets has a pivotal role in Cox-2 induction in monocytes and further supports the key role of platelets in the inflammatory and reparative responses.
Cyclooxygenase‐2 inhibition restores ultraviolet B‐induced downregulation of <i>ATP2A2</i> /SERCA2 in keratinocytes: possible therapeutic approach of cyclooxygenase‐2 inhibition for treatment of Darier disease
Authors: M. Kamijo, C. Nishiyama, A. Takagi, N. Nakano, M. Hara, S. Ikeda, K. Okumura, H. Ogawa
Journal: British Journal of Dermatology (2012)

Journal Article Cyclooxygenase‐2 inhibition restores ultraviolet B‐induced downregulation of ATP2A2/SERCA2 in keratinocytes: possible therapeutic approach of cyclooxygenase‐2 inhibition for treatment of Darier disease Get access M. Kamijo, M. Kamijo Atopy Research Center andDepartment of Dermatology, Juntendo University School of Medicine, 2‐1‐1 Hongo, Bunkyo‐ku, Tokyo 113‐8421, Japan Search for other works by this author on: Oxford Academic Google Scholar C. Nishiyama, C. Nishiyama Atopy Research Center and Chiharu Nishiyama. E‐mail: chinishi@juntendo.ac.jp Search for other works by this author on: Oxford Academic Google Scholar A. Takagi, A. Takagi Department of Dermatology, Juntendo University School of Medicine, 2‐1‐1 Hongo, Bunkyo‐ku, Tokyo 113‐8421, Japan Search for other works by this author on: Oxford Academic Google Scholar N. Nakano, N. Nakano Atopy Research Center and Search for other works by this author on: Oxford Academic Google Scholar M. Hara, M. Hara Atopy Research Center and Search for other works by this author on: Oxford Academic Google Scholar S. Ikeda, S. Ikeda Department of Dermatology, Juntendo University School of Medicine, 2‐1‐1 Hongo, Bunkyo‐ku, Tokyo 113‐8421, Japan Search for other works by this author on: Oxford Academic Google Scholar K. Okumura, K. Okumura Atopy Research Center and Search for other works by this author on: Oxford Academic Google Scholar H. Ogawa H. Ogawa Atopy Research Center and Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 166, Issue 5, 1 May 2012, Pages 1017–1022, https://doi.org/10.1111/j.1365-2133.2011.10789.x Published: 01 May 2012 Article history Accepted: 06 December 2011 Published: 01 May 2012
Lessons Learned From Yet Another Episode of Diethylene Glycol Poisoning
Authors: Jeffrey Brent
Journal: JAMA Internal Medicine (2014)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Internal Medicine journal
Alveolar cell carcinoma complicating sickle cell anemia: A chance occurrence?
Authors: Marlon Labi, Edward F. Haponik, Ronald A. Welsh, Warren R. Summer
Journal: American Journal of Hematology (1989)

Abstract Alveolar cell carcinoma, a neoplasm associated with pre‐existing inflammatory lung disease, has not been reported previously in patients with sickle cell disease. We present such a patient and suggest that chronic pulmonary scarring in this setting predisposed to development of his malignancy. As survival increases in individuals with sickle cell disease, alveolar cell carcinoma must be considered in these differential diagnosis of otherwise unexplained chronic pulmonary infiltrates.
Molecular Pathways: Activating T Cells after Cancer Cell Phagocytosis from Blockade of CD47 “Don't Eat Me” Signals
Authors: Melissa N. McCracken, Adriel C. Cha, Irving L. Weissman
Journal: Clinical Cancer Research (2015)

Abstract Recent advances with immunotherapy agents for the treatment of cancer have provided remarkable, and in some cases, curative results. Our laboratory has identified CD47 as an important “don't eat me” signal expressed on malignant cells. Blockade of the CD47:SIRP-α axis between tumor cells and innate immune cells (monocytes, macrophages, and dendritic cells) increases tumor cell phagocytosis in both solid tumors (including, but not limited to, bladder, breast, colon, lung, and pancreatic) and hematologic malignancies. These phagocytic innate cells are also professional antigen-presenting cells (APC), providing a link from innate to adaptive antitumor immunity. Preliminary studies have demonstrated that APCs present antigens from phagocytosed tumor cells, causing T-cell activation. Therefore, agents that block the CD47:SIRP-α engagement are attractive therapeutic targets as a monotherapy or in combination with additional immune-modulating agents for activating antitumor T cells in vivo. Clin Cancer Res; 21(16); 3597–601. ©2015 AACR.
Mechanism of insulin receptor kinase inhibition in non-insulin-dependent diabetes mellitus patients. Phosphorylation of serine 1327 or threonine 1348 is unaltered.
Authors: M Kellerer, M Coghlan, E Capp, A Mühlhöfer, G Kroder, L Mosthaf, P Galante, K Siddle, H U Häring
Journal: Journal of Clinical Investigation (1995)

The tyrosine kinase activity of insulin receptor isolated from the skeletal muscle of NIDDM patients has previously been found to be decreased compared with the activity of receptor from nondiabetic subjects but the mechanism underlying this defect is unknown. Phosphorylation of receptor serine/threonine residues has been proposed to exert an inhibitory influence on receptor tyrosine kinase activity and Ser 1327 and Thr 1348 have been identified as specific sites of phosphorylation in the insulin receptor COOH terminal domain. To address the potential negative regulatory role of phosphorylation of these residues in vivo, we assessed the extent of phosphorylation of each site in insulin receptor isolated from the skeletal muscle of 12 NIDDM patients and 13 nondiabetic, control subjects. Phosphorylation of Ser 1327 and Thr 1348 was determined using antibodies that specifically recognize insulin receptor phosphorylated at these sites. In addition, a phosphotyrosine-specific antibody was used to monitor receptor tyrosine phosphorylation. The extent of insulin-induced tyrosine autophosphorylation was decreased in receptor isolated from diabetic versus nondiabetic muscle, thus confirming earlier reports. In contrast, there was no significant difference in the extent of phosphorylation of either Ser 1327 or Thr 1348 in receptor isolated from diabetic or nondiabetic muscle as assessed by immunoprecipitation (Ser 1327: 5.6 +/- 1.6% diabetics vs. 4.7 +/- 2.0% control; Thr 1348: 3.8 +/- 1.0% diabetics vs. 3.2 +/- 1.2% control). Moreover, within each group there was no correlation between the level of tyrosine kinase activity and the extent of serine/threonine phosphorylation. It is concluded that the stoichiometry of serine/threonine phosphorylation of insulin receptor in vivo is low, and that increased phosphorylation of Ser 1327 or Thr 1348 is not responsible for the decreased insulin receptor tyrosine kinase activity observed in the skeletal muscle of NIDDM patients.
Anatomic Renal Artery Branch Microdissection to Facilitate Zero-Ischemia Partial Nephrectomy
Authors: Casey K. Ng, Inderbir S. Gill, Mukul B. Patil, Andrew J. Hung, Andre K. Berger, Andre Luis de Castro Abreu, Masahiko Nakamoto, Manuel S. Eisenberg, Osamu Ukimura, Duraiyah Thangathurai, Monish Aron, Mihir M. Desai
Journal: European Urology (2011)
Detection of Associated Ocular Lesions During Screening of Diabetic Retinopathy
Authors: Nilanjana Deb-Joardar, Natacha Germain, Gilles Thuret, Anne-Frédérique Garcin, Pierre Manoli, Bruno Estour, Philippe Gain
Journal: Diabetes Care (2005)

Diabetic retinopathy is the foremost cause of blindness in the working-age population in France (1). An increased incidence of diabetes combined with the lack of ophthalmologists and absence of optometrists makes screening inaccessible to the vast majority. In this setting, the digital fundus camera provides a rapid, sensitive, and cost-effective option (2). Since its installation in our hospital diabetes clinic, patients now routinely undergo photographic screening. Dilated multifield photography allowed good quality imaging of the posterior fundus, which enabled detection of other coexisting pathologies in addition to diabetic retinopathy.

Fundus photographs of 1,153 consecutive patients attending our screening clinic between November 2003 and October 2004 were recorded with the Topcon TRC NW6S camera …
Characterization of the vascular thromboxane A2/prostaglandin endoperoxide receptor in rabbit aorta. Regulation by dexamethasone.
Authors: W C Sessa, P V Halushka, A Okwu, A Nasjletti
Journal: Circulation Research (1990)

Recently, we have shown that dexamethasone treatment of rabbits specifically reduces vascular smooth muscle responsiveness to agonists that interact with the vascular thromboxane A2/prostaglandin H2 (TXA2/PGH2) receptor. One potential site at which dexamethasone can influence prostanoid-mediated vasoconstriction may be at the level of the vascular TXA2/PGH2 receptor. Therefore, we characterized the vascular TXA2/PGH2 receptor in rabbit aortic membranes and examined the influence of dexamethasone treatment on vascular TXA2/PGH2 receptor affinity and number. The binding of [125I][1S-(1 alpha,2 beta(5Z),3 alpha(1E,3R)4 alpha)]-7-[3-(3- hydroxy-4-(p-iodophenoxy)-1-butenyl)-7-oxabicyclo[2.2.1] heptan-2-yl]-5-heptanoic acid ([125I]BOP), a potent TXA2/PGH2 receptor agonist, to rabbit aortic membranes was saturable, displaceable, and dependent on protein concentration. Scatchard analysis of equilibrium binding data disclosed one class of high affinity binding sites with a Kd of 0.44 +/- 0.13 nM and a Bmax of 114.4 +/- 5.2 fmol/mg protein (n = 7). Removal of the endothelium before membrane preparation did not significantly alter the affinity or number of binding sites for [125I]BOP. Kinetic analysis of the rates of [125I]BOP association/dissociation yielded a Kd of 0.62 nM. The ability of various agonists at the TXA2/PGH2 receptor to displace [125I]BOP from vascular membranes correlated well with their contractile potencies in rabbit aortic rings. Moreover, stereospecific displacement of [125I]BOP binding in aortic membranes and inhibition of U46619-mediated aortic contractions were obtained with the stereoisomers L657925(-) and L657926(+). Collectively, these data suggest that this binding site represents the functionally relevant vascular TXA2/PGH2 receptor. In functional experiments, [127I]BOP induced concentration-dependent contractions of the rabbit aorta, which were reduced by 52% in vessels from dexamethasone-treated rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)
Iron loading and the liver: the effect on regeneration after partial hepatectomy
Authors: M. C. Brain
Journal: Gut (1964)

The gain in weight and incidence of mitosis of the posterior lobes of iron-loaded and control rats are compared following partial hepatectomy. The percentage gain in weight of the regenerating livers over the first 72 hours was similar in the two groups, but at 11 days and 12 weeks growth of the iron-loaded livers was less than that of the controls. An increased incidence of mitosis was found in the iron-loaded rats, both before and after partial hepatectomy.
Accuracy of perceptions of hepatitis B and C status: cross sectional investigation of opiate addicts in treatment
Authors: D. Best, A. Noble, E. Finch, M. Gossop, C. Sidwell, J. Strang
Journal: BMJ (1999)

received at the laboratory).Compared with direct immunofluorescence, near patient testing showed a sensitivity of 79% (95% confidence interval 67.3% to 88.5%), a specificity of 97% (82.8% to 99.9%), a positive predictive value of 98% (89.6% to 99.9%), and a negative predictive value of 70% (53.9% to 82.8%).Near patient testing proved acceptable to the staff performing it, and it was well received in the hospital wards in terms of facilitating patient management and infection control.
Rheumatoid factor determines structural progression of rheumatoid arthritis dependent and independent of disease activity
Authors: Daniel Aletaha, Farideh Alasti, Josef S Smolen
Journal: Annals of the Rheumatic Diseases (2012)

Background Rheumatoid factor (RF) is prototypic for rheumatoid arthritis (RA) and serves diagnostic and prognostic purposes. RF is associated with joint destruction, but the role of disease activity as a potential mediator of these effects has not been clearly elucidated yet. Objective To investigate if higher radiographic progression (Sharp score, ΔTSS) in RF+ patients is dependent or independent of disease activity. Methods The authors performed a cross-sectional multivariate analysis at baseline and a matched cohort study in patients from five RA clinical trials. The authors pooled methotrexate treatment arms and compared ΔTSS in RF+ and RF− patients before and after matching for other associated variables. Results Among 686 patients, 124 were RF− and 562 RF+, 343 having high (&gt;160 U/ml) RF. ΔTSS was 1.03±5.83, 3.23±8.10 and 3.58±8.18 (p&lt;0.0001), respectively, and similarly for erosions and joint space narrowing (JSN). After matching for other prognostically important variables, ΔTSS still was lower among 61 RF− versus 61 RF high+ patients (0.52±2.47 vs 3.09±8.28; p=0.028), mainly related to differences in erosion score (0.31±1.88 vs 2.07±5.62; p=0.035), but not JSN (0.21±1.26 vs 1.02±3.31; p=0.162). Conclusions The data reveal that damage progression in seropositive RA patients is related to higher levels of disease activity and to independent effects of RF, particularly on bone damage. This calls for consideration of RF status irrespective of disease activity.
Small Nucleolar RNAs U32a, U33, and U35a Are Critical Mediators of Metabolic Stress
Authors: Carlos I. Michel, Christopher L. Holley, Benjamin S. Scruggs, Rohini Sidhu, Rita T. Brookheart, Laura L. Listenberger, Mark A. Behlke, Daniel S. Ory, Jean E. Schaffer
Journal: Cell Metabolism (2011)
Vitamin D inhibits proliferation and profibrotic marker expression in hepatic stellate cells and decreases thioacetamide-induced liver fibrosis in rats
Authors: S. Abramovitch, L. Dahan-Bachar, E. Sharvit, Y. Weisman, A. B. Tov, E. Brazowski, S. Reif
Journal: Gut (2011)

<h3>Background and aim</h3> Hepatic stellate cells (HSCs) are key participants in liver fibrosis development. 1,25(OH)<sub>2</sub>D<sub>3</sub>, the active form of vitamin D, has antiproliferative properties and antifibrotic potential, as well as a role in extracellular matrix and matrix metalloproteinase (MMP) regulation in renal and lung fibrosis. Little is known about the role of 1,25(OH)<sub>2</sub>D<sub>3</sub> in liver and its involvement in liver fibrosis. Therefore, we investigated the antiproliferative and antifibrotic effects of 1,25(OH)<sub>2</sub>D<sub>3</sub> in primary cultured HSCs and in a rat model of liver fibrosis induced by thioacetamide (TAA). <h3>Methods</h3> Primary HSCs were isolated from rats9 livers and treated with 1,25(OH)<sub>2</sub>D<sub>3</sub>. Proliferation was examined by bromodeoxyuridine. Vitamin D receptor (VDR) expression and several fibrotic markers were detected by western blot analysis and real-time PCR. Collagen Iα1 and MMP-9 promoter activity were measured by luciferase assay. MMP-9 enzymatic activity was investigated by zymography. VDR silencing was performed by sh-RNA. An in vivo study was performed on TAA-induced liver fibrosis model in rats treated with or without 1,25(OH)<sub>2</sub>D<sub>3</sub>. The fibrotic score and collagen deposition were determined by Masson and by Sirius red staining. <h3>Results</h3> While VDR was highly expressed in quiescent HSCs, its expression decreased up to 40% during activation. Addition of 1,25(OH)<sub>2</sub>D<sub>3</sub> to activated HSCs stimulated VDR expression. 1,25(OH)<sub>2</sub>D<sub>3</sub> suppressed HSC proliferation and cyclin D1 expression by ∼50% and tissue inhibitor of metalloproteinase 1 (TIMP-1) by 60% and led to a 40% downregulation of collagen Iα1 expression. Moreover, 1,25(OH)<sub>2</sub>D<sub>3</sub> increased MMP-9 activity by 30%. Silencing VDR by sh-RNA demonstrated that suppression of cyclin D1 and collagen Iα1 protein expression was VDR dependent. Treatment with 1,25(OH)<sub>2</sub>D<sub>3</sub> significantly reduced extracellular matrix deposition and lowered the fibrotic score in TAA-induced liver fibrosis. <h3>Conclusion</h3> 1,25(OH)<sub>2</sub>D<sub>3</sub> has antiproliferative and antifibrotic effects on liver fibrosis in in vitro and in vivo models and may be considered as having potential therapeutic value.