Tim Scholz

Medizinische Hochschule Hannover

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i-10 index

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Ansgar O. Aasen

Oslo University Hospital

Bernhard Brenner

Medizinische Hochschule Hannover

P. Jørgensen

Norwegian University of Science and Technology

Yngvar Gundersen

Norwegian Defence Research Establishment

Mamta Amrute‐Nayak

Medizinische Hochschule Hannover

ØM

Øystein Mathisen

Oslo University Hospital

Vibeke Videm

Norwegian University of Science and Technology

Theresia Kraft

Medizinische Hochschule Hannover

OØ

Ole Øyen

Oslo University Hospital

Jørn A. Holme

Norwegian Institute of Public Health

Cooperative Institutions

Oslo University Hospital

University of Oslo

Medizinische Hochschule Hannover

Goethe University Frankfurt

University College London

University Hospital Regensburg

Heidelberg University

National Hospital for Neurology and Neurosurgery

Med-Storm Innovation (Norway)

University Hospital Frankfurt

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Sirolimus Interferes with the Innate Response to Bacterial Products in Human Whole Blood by Attenuation of IL‐10 Production

Scandinavian Journal of Immunology (2001)

P. Jørgensen J. E. Wang Mia Almlöf Rigmor Solberg Cecilie Okkenhaug

Current immunosuppressive strategies are aimed at abrogating the allospecific T‐cell response against donor tissues or organs. However, little information is yet available on the potential influences of these drugs on innate immune responses. In order to address this, we have employed a whole blood model. Human whole blood was pretreated with sirolimus, cyclosporine A or tacrolimus in therapeutic as well as supra therapeutic doses, and subsequently stimulated with lipopolysaccharide (LPS), peptidoglycan (PepG) or lipoteichoic acid (LTA). Plasma cytokine analyses revealed a potent inhibitory effect of sirolimus on interleukin(IL)‐10 production induced by all bacterial products tested. In contrast, cyclosporine A and tacrolimus inhibited the tumour necrosis factor (TNF)‐α production in response to LPS, but not to PepG and LTA. Using a quantitative mRNA analyses, we also observed that sirolimus significantly decreased the IL‐10 mRNA accumulation to sub‐basal levels in peripheral blood mononuclear cells (PBMC). This suggests that the sirolimus inhibits IL‐10 production by interfering with the IL‐10 gene transcription. However, the molecular mechanism of this inhibition remains unclear. Based on the present study and observations by others, we postulate that the clinical use of the sirolimus may be associated with a dysregulated innate immune response to bacterial infection and thus an increased risk of hyperinflammation and sepsis.

Lipoteichoic acid

Sirolimus

10.1046/j.1365-3083.2001.00862.x

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Citations (44)

Phosphoinositide-Mediated Myosin-1 Membrane Targeting during Endocytosis

Biophysical Journal (2018)

Girish Rajendraprasad Tim Scholz Matthias Preller Georgios Tsiavaliaris

10.1016/j.bpj.2017.11.252

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Citations (2)

Nitric oxide synthase inhibition reduces venous return in porcine endotoxemia

AJP Heart and Circulatory Physiology (1996)

T. Sætre O A Smiseth Tim Scholz Hege S. Carlsen Lars Nordsletten

Mechanisms of circulatory effects induced by nitric oxide synthase inhibition in endotoxemia were investigated in 36 pigs randomized to 1) endotoxin infusion (1.7 micrograms.kg-1.h-1 iv) for 7 h and bolus NG-nitro-L-arginine methyl ester (L-NAME; 25 mg/kg iv) after 3 h; 2) endotoxin infusion for 7 h; 3) saline infusion for 7 h and L-NAME after 3 h; and 4) saline infusion for 7 h. Fifteen minutes after L-NAME injection during endotoxemia, reductions in cardiac output (41%, P < 0.05), portal venous flow (51%, P < 0.05), and hepatic artery flow (50%, P < 0.05) were observed. Systemic vascular resistance increased by 82% (P < 0.05), and the portocaval vascular resistance increased by 101% (P < 0.05). Despite marked vasoconstriction after L-NAME, left ventricular intracavitary filling pressure, central venous pressure, and arterial pressure remained unchanged. During endotoxemia, hematocrit increased from 38.4 +/- 1.4 to 41.9 +/- 1.2 after L-NAME, and blood volume (n = 3) was reduced by an average of 8.3 ml/kg body wt. These changes probably reflect transcapillary fluid loss as urine output was unchanged. In conclusion, L-NAME decreased intravascular blood volume and increased splanchnic venous resistance. These effects will tend to reduce venous return. Combined with a marked increase in left ventricular after-load, L-NAME may thus compromise cardiovascular function in endotoxemia.

Bolus (digestion)

Venous return curve

10.1152/ajpheart.1996.271.4.h1325

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Citations (16)

Myosin-1 Function Extends to Microtubule-Dependent Processes

Biophysical Journal (2010)

Tim Scholz Agrani Rump Petra Uta Maike H. Hinrichs Claudia Thiel

Kinesin

Molecular motor

Organelle

Actin remodeling

10.1016/j.bpj.2009.12.3040

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Citations (1)

Prophylactic Peritoneal Fenestration to Prevent Morbidity After Kidney Transplantation: A Randomized Study

Transplantation (2011)

Trygve Syversveen Karsten Midtvedt Knut Brabrand Ole Øyen Aksel Foss

Formation of lymphocele (accumulation of lymphatic fluid) is a common surgical complication following kidney transplantation. This open randomized trial evaluated the effect of prophylactic fenestration on lymphocele formation.Adult recipients of kidney grafts from deceased donors were randomized to undergo peritoneal fenestration during the transplantation or to standard surgical procedure without fenestration. The incidence of symptomatic lymphocele in the two groups was compared at 1 year after transplantation. A protocol-based ultrasound examination was performed in the 1st, 5th, and 10th postoperative week. Any hypoechoic perirenal collection was registered.One hundred thirty recipients were randomized to peritoneal fenestration (n = 69) or standard therapy (n = 61). Six patients were excluded. Nine of 58 (15.5%) patients in the standard group developed symptomatic lymphoceles requiring treatment during the first postoperative year, versus 2 of 66 (3.0%) in the fenestration group (relative risk = 0.20, 95% confidence interval: 0.04-0.82, P = 0.015). Seven major surgical procedures and five percutaneous drainages due to lymphoceles were performed in the standard group, compared with two percutaneous drainages in the fenestration group. The prevalence of fluid collections in the fifth postoperative week was significantly higher in the standard group (66% vs. 37%; relative risk = 0.57, 95% confidence interval: 0.37-0.71, P = 0.005).Prophylactic fenestration reduced the risk of lymphoceles and the need for invasive procedures to treat this condition. The results need to be confirmed in a population of transplant recipients on lower steroids and with the use of wound drains.

Lymphocele

10.1097/tp.0b013e318220f57b

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Citations (18)

Heparin coating reduces cell activation and mediator release in an in vitro venovenous bypass model for liver transplantation

Transplant International (1998)

Rigmor Solberg Tim Scholz Vibeke Videm Cecilie Okkenhaug Ansgar O. Aasen

Monocyte

Interleukin 8

10.1111/j.1432-2277.1998.tb00966.x

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Citations (31)

Publisher's Note: Three-dimensional bead position histograms reveal single-molecule nanomechanics [Phys. Rev. E71, 021907 (2005)]

Physical Review E (2005)

Nils B. Becker Stephan Altmann Tim Scholz J. K. H. Hörber Ernst H. K. Stelzer

Nanomechanics

Bead

Position (finance)

10.1103/physreve.71.039905

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Citations (0)

Actin sliding on reconstituted myosin filaments containing only one myosin heavy chain isoform.

Journal of Muscle Research and Cell Motility (2003)

Tim Scholz Bernhard Brenner

Meromyosin

10.1023/a:1024871825135

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Citations (13)

PRETREATMENT WITH THE SELECTIVE NITRIC OXIDE SYNTHASE INHIBITOR AMINOETHYL-ISOTHIOUREA IN PORCINE ENDOTOXEMIA

Shock (1997)

Yngvar Gundersen T. Sætre Tim Scholz Per Lilleaasen Ansgar O. Aasen

10.1097/00024382-199703001-00276

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Citations (0)

The NO Donor Sodium Nitroprusside Reverses the Negative Effects on Hepatic Arterial Flow Induced by Endotoxin and the NO Synthase Inhibitor L-NAME

European Surgical Research (1996)

Yngvar Gundersen T. S aelig tre Tim Scholz Hege S. Carlsen Harald Kjekshus

In previous studies we have observed that the nitric oxide synthase inhibitor L-NAME induces a profound deterioration of liver circulation in experimental endotoxemia. Using the same porcine model we now have evaluated the possibility of modulating these effects with the nitric oxide donor sodium nitroprusside. Infusion of endotoxin led to a gradual deterioration of hemodynamic parameters, including liver blood flow. The decreases in portal blood flow paralleled and matched the decreases in cardiac output, and no compensatory increase in hepatic arterial flow occurred. L-NAME had detrimental effects on hemodynamics, including the liver circulation. The latter effects could, however, partially be reversed by sodium nitroprusside. Hepatic arterial flow increased from 1.9 to 7.2 ml/kg/min, with a concomitant decrease in hepatic arterial resistance from 5,364 to 1,746 dyn s/cm5 kg. A control group exhibited no significant change in either flow or resistance. The response to sodium nitroprusside was rapid and vigorous, and probably largely due to relaxation of the hepatic arterioles, and not to abatement of intrahepatic edema or plugging of the sinusoids. Furthermore, we conclude that the endotoxin-induced dysfunction of the hepatic arterial buffer response may be due to a selective inhibition of vascular endothelial function.

Sodium nitroprusside

10.1159/000129473

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Citations (20)