scholarly journals No proof for retinal amyloid after oral curcumin in amyloid confirmed AD cases

2021 ◽  
Author(s):  
Jurre den Haan ◽  
Frederique J. Hart de Ruyter ◽  
Benjamin Lochocki ◽  
Maurice A.G.M. Kroon ◽  
E. Marleen Kemper ◽  
...  
Keyword(s):  
Plasma Levels ◽  
Visual Assessment ◽  
Autofluorescence Imaging ◽  
Quantitative Analyses

AbstractINTRODUCTIONPrevious work showed in-vivo presence of retinal amyloid in AD patients using curcumin. We aimed to replicate these findings in an amyloid biomarker confirmed cohort.METHODSTwenty-six AD patients (age 66 (±9), MMSE≥18) and 14 controls (age 71(±12)) used three curcumin formulations: Longvida®, Theracurmin® and Novasol®. Plasma levels were determined and pre- and post-curcumin retinal scans acquired using autofluorescence imaging. Images were both visually and quantitatively assessed.RESULTSVisual assessment showed no difference between AD patients and controls for pre- and post-curcumin images. This was confirmed by quantitative analyses. Mean plasma curcumin levels were 198.7 nM (Longvida®), 576.6 nM (Theracurmin®) and 1605.8 nM (Novasol®).DISCUSSIONWe found no difference in retinal focal fluorescence in an amyloid biomarker confirmed cohort of AD patients and controls, using Longvida® (previously used for this purpose) and two additional curcumin formulations yielding higher curcumin plasma levels. We therefore question the presence of retinal amyloid.

Plasminogen Activation In Vivo upon Intravenous Infusion of DDAVP

1992 ◽  
Vol 67 (01) ◽  
pp. 111-116 ◽  
Author(s):  
Marcel Levi ◽  
Jan Paul de Boer ◽  
Dorina Roem ◽  
Jan Wouter ten Cate ◽  
C Erik Hack
Keyword(s):  
Monoclonal Antibodies ◽  
Plasminogen Activator ◽  
Plasma Levels ◽  
Fold Increase ◽  
Fibrinolytic System ◽  
Plasminogen Activation ◽  
Plasminogen Activator Activity ◽  
Insight Into

SummaryInfusion of desamino-d-arginine vasopressin (DDAVP) results in an increase in plasma plasminogen activator activity. Whether this increase results in the generation of plasmin in vivo has never been established.A novel sensitive radioimmunoassay (RIA) for the measurement of the complex between plasmin and its main inhibitor α2 antiplasmin (PAP complex) was developed using monoclonal antibodies preferentially reacting with complexed and inactivated α2-antiplasmin and monoclonal antibodies against plasmin. The assay was validated in healthy volunteers and in patients with an activated fibrinolytic system.Infusion of DDAVP in a randomized placebo controlled crossover study resulted in all volunteers in a 6.6-fold increase in PAP complex, which was maximal between 15 and 30 min after the start of the infusion. Hereafter, plasma levels of PAP complex decreased with an apparent half-life of disappearance of about 120 min. Infusion of DDAVP did not induce generation of thrombin, as measured by plasma levels of prothrombin fragment F1+2 and thrombin-antithrombin III (TAT) complex.We conclude that the increase in plasminogen activator activity upon the infusion of DDAVP results in the in vivo generation of plasmin, in the absence of coagulation activation. Studying the DDAVP induced increase in PAP complex of patients with thromboembolic disease and a defective plasminogen activator response upon DDAVP may provide more insight into the role of the fibrinolytic system in the pathogenesis of thrombosis.

scholarly journals Enhancement and Segmentation Workflow for the Developing Zebrafish Vasculature

2019 ◽  
Vol 5 (1) ◽  
pp. 14 ◽  
Author(s):  
Elisabeth Kugler ◽  
Karen Plant ◽  
Timothy Chico ◽  
Paul Armitage
Keyword(s):  
Open Source Software ◽  
Light Sheet ◽  
Visual Assessment ◽  
Cardiovascular Development ◽  
Fluorescent Reporter ◽  
Enhancement Method ◽  
Vertebrate Model ◽  
Vascular Enhancement ◽  
Light Sheet Fluorescence Microscopy

Zebrafish have become an established in vivo vertebrate model to study cardiovascular development and disease. However, most published studies of the zebrafish vascular architecture rely on subjective visual assessment, rather than objective quantification. In this paper, we used state-of-the-art light sheet fluorescence microscopy to visualize the vasculature in transgenic fluorescent reporter zebrafish. Analysis of image quality, vascular enhancement methods, and segmentation approaches were performed in the framework of the open-source software Fiji to allow dissemination and reproducibility. Here, we build on a previously developed image processing pipeline; evaluate its applicability to a wider range of data; apply and evaluate an alternative vascular enhancement method; and, finally, suggest a work-flow for successful segmentation of the embryonic zebrafish vasculature.

Oral N-acetylcysteine protects against perfluoroisobutene toxicity in rats

1997 ◽  
Vol 16 (4) ◽  
pp. 212-216 ◽  
Author(s):  
Alison F Lailey
Keyword(s):  
Oral Administration ◽  
Pulmonary Oedema ◽  
Plasma Levels ◽  
Pyrolysis Product ◽  
Lavage Fluid ◽  
Lethal Effects ◽  
Duration Of Protection ◽  
Gas Exposure

1 Perfluoroisobutene, a pyrolysis product of polytetra fluoroethene may cause pulmonary oedema and death when inhaled. Oral N-acetylcysteine has shown protection against inhalation of perfluoroisobutene and in this study we have tried to elucidate the mechanism by which protection is mediated. 2 Protection against the lethal effects of inhaled per fluoroisobutene has been shown when N-acetylcys teine has been orally administered 4, 6 or 8 h before gas exposure. 3 Plasma levels of cysteine, glutathione and N-acetylcys teine were increased for up to 7 h following oral administration of Nac. 4 N-acetylcysteine was not detected in the bronchio alveolar lavage fluid following oral administration. 5 Duration of protection in vivo has been related to the duration of increased thiol levels in the plasma.

Role of adenosine in noradrenergic neurotransmission in spontaneously hypertensive rats

1987 ◽  
Vol 253 (4) ◽  
pp. H909-H918 ◽  
Author(s):  
E. K. Jackson
Keyword(s):  
Plasma Levels ◽  
Spontaneously Hypertensive Rat ◽  
Base Line ◽  
Inhibitory Effects ◽  
Spontaneously Hypertensive ◽  
Vascular Responses ◽  
Rat Mesentery ◽  
Wistar Kyoto

The purpose of this study was to compare the in vivo role of adenosine as a modulator of noradrenergic neurotransmission in the spontaneously hypertensive rat (SHR) and Wistar-Kyoto control rat (WKY). In the in situ blood-perfused rat mesentery, vascular responses to periarterial (sympathetic) nerve stimulation (PNS) and to exogenous norepinephrine (NE) were enhanced in SHR compared with WKY. In both SHR and WKY, vascular responses to PNS were more sensitive to inhibition by adenosine than were responses to NE. At matched base-line vascular responses, compared with WKY, SHR were less sensitive to the inhibitory effects of adenosine on vascular responses to PNS, but SHR and WKY were equally sensitive with respect to adenosine-induced inhibition of responses to NE. Antagonism of adenosine receptors with 1,3-dipropyl-8-p-sulfophenylxanthine shifted the dose-response curve to exogenous adenosine sixfold to the right yet did not influence vascular responses to PNS or NE in either SHR or WKY. Furthermore, PNS did not alter either arterial or mesenteric venous plasma levels of adenosine in SHR or WKY, and plasma levels of adenosine in both strains were always lower than the calculated threshold level required to attenuate neurotransmission. It is concluded that in vivo 1) exogenous adenosine interferes with noradrenergic neurotransmission in both SHR and WKY; 2) SHR are less sensitive to the inhibitory effects of exogenous adenosine on noradrenergic neurotransmission than are WKY; 3) endogenous adenosine does not play a role in modulating neurotransmission in either strain under the conditions of this study; and 4) enhanced noradrenergic neurotransmission in the SHR is not due to defective modulation of neurotransmission by adenosine.

scholarly journals Increased tissue factor expression on circulating monocytes in chronic HIV infection: relationship to in vivo coagulation and immune activation

Blood ◽  
2010 ◽  
Vol 115 (2) ◽  
pp. 161-167 ◽  
Author(s):  
Nicholas T. Funderburg ◽  
Elizabeth Mayne ◽  
Scott F. Sieg ◽  
Robert Asaad ◽  
Wei Jiang ◽  
...  
Keyword(s):  
Hiv Infection ◽  
Tissue Factor ◽  
Immune Activation ◽  
Interleukin 6 ◽  
Plasma Levels ◽  
Thrombus Formation ◽  
Hiv Replication ◽  
Increased Risk

Abstract HIV infection is associated with an increased risk of thrombosis; and as antiretroviral therapy has increased the lifespan of HIV-infected patients, their risk for cardiovascular events is expected to increase. A large clinical study found recently that all-cause mortality for HIV+ patients was related to plasma levels of interleukin-6 and to D-dimer products of fibrinolysis. We provide evidence that this elevated risk for coagulation may be related to increased proportions of monocytes expressing cell surface tissue factor (TF, thromboplastin) in persons with HIV infection. Monocyte TF expression could be induced in vitro by lipopolysaccharide and flagellin, but not by interleukin-6. Monocyte expression of TF was correlated with HIV levels in plasma, with indices of immune activation, and with plasma levels of soluble CD14, a marker of in vivo lipopolysaccharide exposure. TF levels also correlated with plasma levels of D-dimers, reflective of in vivo clot formation and fibrinolysis. Thus, drivers of immune activation in HIV disease, such as HIV replication, and potentially, microbial translocation, may activate clotting cascades and contribute to thrombus formation and cardiovascular morbidities in HIV infection.

MEDROXYPROGESTERONE ACETATE (MPA) INCREASES PAI-1 SECRETION FROM HUVEC AND ELEVATES THE PLASMA-LEVELS OF PAI-I IN-VIVO

1994 ◽  
Author(s):  
K SERIZAWA ◽  
T URANO ◽  
Y KOJIMA ◽  
H IHARA ◽  
Y TAKADA ◽  
...  
Keyword(s):  
Medroxyprogesterone Acetate ◽  
Plasma Levels ◽  
Pai 1

scholarly journals High-Resolution Adaptive Optics in Vivo Autofluorescence Imaging in Stargardt Disease

2019 ◽  
Vol 137 (6) ◽  
pp. 603 ◽  
Author(s):  
Hongxin Song ◽  
Ethan A. Rossi ◽  
Qiang Yang ◽  
Charles E. Granger ◽  
Lisa R. Latchney ◽  
...  
Keyword(s):  
High Resolution ◽  
Adaptive Optics ◽  
Autofluorescence Imaging ◽  
Stargardt Disease

scholarly journals Optimization of In Vivo Confocal Autofluorescence Imaging of the Ocular Fundus in Mice and Its Application to Models of Human Retinal Degeneration

2012 ◽  
Vol 53 (2) ◽  
pp. 1066 ◽  
Author(s):  
Peter Charbel Issa ◽  
Mandeep S. Singh ◽  
Daniel M. Lipinski ◽  
Ngaihang V. Chong ◽  
François C. Delori ◽  
...  
Keyword(s):  
Retinal Degeneration ◽  
Autofluorescence Imaging ◽  
Ocular Fundus

Increase of Thrombin-Antithrombin III (TAT) Complex Plasma Levels in Thromboembolic Diseases during Thrombolysis

1987 ◽  
Author(s):  
R Seitz ◽  
G Pratorius ◽  
R Blanke ◽  
B B Strauer
Keyword(s):  
Thrombolytic Therapy ◽  
Plasma Levels ◽  
Vein Thrombosis ◽  
Complex Plasma ◽  
In Vitro Effects ◽  
Immuno Assay ◽  
Enzyme Immuno Assay ◽  
Deep Vein

Recently an enzyme immuno assay of thrombin-antithrombinlll complex (TAT) plasma levels was developed by PELZER et al. (Thromb. Haemost. 54:24,1985). This test appears to be useful in the detection of intravasal thrombin generation, since all of 17 patients (pts.) with pulmonary embolism and 15 of 16 pts. with deep vein thrombosis (DVT) showed elevated values above 3 ng/ml.In 9 pts. with acute myocardial infarction (AMI) the TAT levels increased significantly (p 0.001) 3 to 6 hours after thrombolytic therapy with 1.5 million units streptokinase (SK) over 30 minutes. A concomitant increase of fibrinopeptide A (FPA) levels (p=0.048) was observed. In contrast, 8 AMI pts. treated with heparin showed an insignificant increase of TAT and FPA. In 7 DVT pts. the TAT levels rose significantly (p 0.001) within 6 hours after start of urokinase (UK) infusion, while the FPA levels were enhanced prior to treatment and showed no further increase.In order to assess the in vitro effects of SK and UK on TAT levels, clots obtained by recalcification of citrated plasma were incubated in heparin (2 units/ml) plasma. An increase of TAT occurred after addition of SK or UK, which was less pronounced when the clots were rinsed extensivly or squeezed before incubation. When SK or UK were added to plasma in the absence of a clot, still a small increase of TAT occurred which was absent in saline controls.The data suggest that SK and UK action is associated with the generation of TAT complexes. In vivo, thrombin or thromboplastic material might be released by enhanced "wash out" from the recanalized coronary artery or from the reperfused in-farcted myocardium. Thrombin might also be released from binding sites on fibrin clots or fibrinogen. It is conceivable that these findings contribute to the understanding of reocclusion of infarct vessels after thrombolytic therapy. This points to the importance of careful anticoagulation in patients receiving thrombolytic therapy.

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