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1.  Differential in vivo activation of monocyte subsets during low-grade inflammation through experimental endotoxemia in humans 
Scientific Reports  2016;6:30162.
Human monocytes are a heterogeneous cell population, which can be divided into a classical (CD14++CD16−), a non-classical (CD14+CD16+), and an intermediate (CD14++CD16+) subset. We hypothesized that low-grade inflammation may differentially affect monocyte subsets. We used a human lipopolysaccharide (LPS) infusion model to mimic low-grade inflammation to identify, which monocyte subsets are preferentially activated under these conditions. Monocyte subsets were identified by staining for CD14 and CD16, activation status of monocytes was analyzed by staining for CD11b and a novel in situ mRNA hybridization approach to detect IL-6 and IL-8 specific mRNA at the single-cell level by flow cytometry. After LPS challenge, cell numbers of monocyte subsets dropped after 2 h with cell numbers recovering after 6 h. Distribution of monocyte subsets was skewed dramatically towards the intermediate subset after 24 h. Furthermore, intermediate monocytes displayed the largest increase of CD11b expression after 2 h. Finally, IL-6 and IL-8 mRNA levels increased in intermediate and non-classical monocytes after 6 h whereas these mRNA levels in classical monocytes changed only marginally. In conclusion, our data indicates that the main responding subset of monocytes to standardized low-grade inflammation induced by LPS in humans is the CD14++CD16+ intermediate subset followed by the CD14+CD16+ non-classical monocyte subset. Circulating classical monocytes showed comparably less reaction to LPS challenge in vivo.
PMCID: PMC4957086  PMID: 27444882
2.  The inflammatory mediator oncostatin M induces angiopoietin 2 expression in endothelial cells in vitro and in vivo 
Members of the glycoprotein 130 (gp130) receptor–gp130 ligand family play a role in angiogenesis in different tissues. We tested the effect of this cytokine family on the angiopoietin (Ang)–Tie system, which is involved in blood vessel maturation, stabilization, and regression.
Oncostatin M (OSM) increased Ang2 expression in human umbilical vein endothelial cells via Janus kinase/signal transducer and activator of transcription (JAK/STAT) and mitogen-activated protein (MAP) kinase activation. Furthermore, OSM induced Ang2 expression in macrovascular endothelial cells isolated from the human aorta and in microvascular endothelial cells isolated from human heart. Our in vivo experiments revealed that mRNA expression of Ang2 in hearts of mice injected with OSM increased significantly, and levels of OSM mRNA significantly correlated with mRNA levels of Ang2 in human hearts. In addition, OSM increased the expression of its own receptors, gp130 and OSM receptor, in endothelial cells in vitro and in mice in vivo, and levels of OSM mRNA significantly correlated with mRNA levels of gp130 and OSM receptor in human hearts.
Our data, showing the effects of OSM on the Ang–Tie system in endothelial cells, in hearts of mice, and in human heart tissue, provide yet another link between inflammation and angiogenesis.
PMCID: PMC2857505  PMID: 20088942
angiogenesis; angiopoietin; cytokine; oncostatin M
3.  No evidence for a direct role of Helicobacter pylori and Mycoplasma pneumoniae in carotid artery atherosclerosis 
Journal of Clinical Pathology  2006;59(11):1186-1190.
That infections with certain pathogens, by initiating an inflammatory response, may contribute to the development of atherosclerosis is suggested by clinical and experimental evidence.
To analyse atherosclerotic plaques of the carotid artery, samples of apparently healthy greater saphenous veins and circulating leucocytes from the same individual patients for the presence of Helicobacter pylori and Mycoplasma pneumoniae.
Samples from 36 patients undergoing carotid endarterectomy for symptomatic carotid artery stenosis were analysed by polymerase chain reaction for the presence of DNA specific for H pylori and M pneumoniae. IgG antibody titres against H pylori and M pneumoniae and plasma levels of soluble E‐selectin, soluble intercellular adhesion molecule‐1 and soluble vascular cell adhesion molecule‐1 were determined.
M pneumoniae‐specific DNA was detected in the atherosclerotic plaques of 13 of 36 (36.1%) patients, in the saphenous veins of 9 of 36 (25%) patients and in the leucocytes of 27 of 36 (75%) patients. No salient association was observed between the presence of M pneumoniae‐specific DNA in leucocytes and atherosclerotic plaques or veins. A marked correlation between the presence of M pneumoniae in the respective specimens and the studied inflammatory markers or the presence of anti‐M pneumoniae antibodies was not observed. H pylori‐specific DNA could not be detected in the specimens tested.
The absence of H pylori and the random distribution of M pneumoniae in tissue samples obtained from patients with symptomatic carotid artery stenosis do not support a role for these pathogens in the development of atherosclerosis due to a direct interaction of the bacteria with the vasculature.
PMCID: PMC1860507  PMID: 16644879
4.  Revascularization alone or combined with suture annuloplasty for ischemic mitral regurgitation. Evaluation by color Doppler echocardiography. 
Texas Heart Institute Journal  1996;23(4):270-278.
To determine the effectiveness of revascularization alone or combined with mitral valve repair for ischemic mitral regurgitation, we performed color Doppler echocardiography intraoperatively before and after cardiopulmonary bypass in 49 patients (mean age, 70 +/- 9 years) with concomitant mitral regurgitation and coronary artery disease (triple vessel or left main in 88%; prior infarction in 90%). After revascularization alone (n = 25), the mitral annulus diameter (2.88 +/- 0.44 cm vs 2.88 +/- 0.44 cm), leaflet-to-annulus ratio (1.44 +/- 0.30 vs 1.44 +/- 0.29), and mitral regurgitation grade (1.7 +/- 0.9 vs 1.8 +/- 0.7) remained unchanged (p = NS, postpump vs prepump); mitral regurgitation decreased by 2 grades in only 1 patient (4%). After combined revascularization and mitral valve suture annuloplasty (Kay-Zubiate; n = 24), the annulus diameter decreased (to 2.57 +/- 0.45 cm from 3.11 +/- 0.43 cm), the leaflet-to-annulus ratio increased (to 1.46 +/- 0.25 from 1.20 +/- 0.21), and the mitral regurgitation grade decreased significantly (to 0.9 +/- 0.9 from 2.8 +/- 1.0) (p < 0.01); mitral regurgitation decreased by 2 grades or more (successful repair) in 75%. The origin of the jet correlated with the site of prior infarction (p < 0.05), being inferior in cases of posterior or inferior infarction (67%), and central or broad in cases of combined anterior and inferior infarction (70%). Despite a slightly higher 30-day mortality in the repair group (p = 0.10), there was no significant difference in survival between the 2 surgical groups at 5 years or 8 years. Therefore, in this study of patients with mitral regurgitation and coronary artery disease, reduction in regurgitation grade with revascularization alone was infrequent. Concomitant suture annuloplasty significantly reduced regurgitation by reestablishing a more normal relationship between the leaflet and annulus sizes. The failure rate after suture annuloplasty was 25%; alternative repair techniques such as ring annuloplasty may have a lower failure rate.
PMCID: PMC325370  PMID: 8969026
5.  The Treatment of the Incomplete Pneumothorax 
The Ulster Medical Journal  1937;6(3):170-179.
PMCID: PMC2479125  PMID: 20476128
6.  The Treatment of Pleural Effusions 
PMCID: PMC2075889  PMID: 19991114
British Medical Journal  1929;1(3566):849.
PMCID: PMC2450941  PMID: 20774664

Results 1-7 (7)