Publications by authors named "Veldman M"

61 Publications

Stem cells on fire: inflammatory signaling in HSC emergence.

Dev Cell 2014 Dec;31(5):517-8

Department of Molecular, Cell and Developmental Biology, UCLA, Los Angeles, CA 90095, USA. Electronic address:

Inflammatory pathways protect the body from infection and promote healing following injury. Recent reports demonstrate the surprising involvement of these pathways during hematopoietic stem cell emergence from the hemogenic endothelium in both zebrafish and mice.
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http://dx.doi.org/10.1016/j.devcel.2014.11.026DOI Listing
December 2014

Direct and crossed effects of somatosensory stimulation on neuronal excitability and motor performance in humans.

Neurosci Biobehav Rev 2014 Nov 23;47:22-35. Epub 2014 Jul 23.

Center for Human Movement Sciences, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands; Faculty of Health and Life Sciences, Northumbria University, Newcastle-upon-Tyne, UK. Electronic address:

This analytic review reports how prolonged periods of somatosensory electric stimulation (SES) with repetitive transcutaneous nerve stimulation can have 'direct' and 'crossed' effects on brain activation, corticospinal excitability, and motor performance. A review of 26 studies involving 315 healthy and 78 stroke and dystonia patients showed that the direct effects of SES increased corticospinal excitability up to 40% (effect size: 0.2 to 6.1) and motor performance up to 14% (effect size: 0.3 to 3.1) but these two features did not correlate. SES did not affect measures of intracortical excitability. Most likely, a long-term potentiation-like mechanism in the excitatory glutamatergic connections between the primary sensory and motor cortices mediates the direct effects of SES on corticospinal excitability and motor performance. We propose two models for the untested hypothesis that adding SES to unilateral motor practice could magnify the magnitude of inter-limb transfer. If tenable, the hypothesis would expand the evolving repertoire of sensory augmentation of cross-education using mirrors and add SES as an alternative to conventional rehabilitation strategies such as constraint-induced movement therapy.
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http://dx.doi.org/10.1016/j.neubiorev.2014.07.013DOI Listing
November 2014

Transdifferentiation of fast skeletal muscle into functional endothelium in vivo by transcription factor Etv2.

PLoS Biol 2013 18;11(6):e1001590. Epub 2013 Jun 18.

State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University, Chengdu, Sichuan, People's Republic of China.

Etsrp/Etv2 (Etv2) is an evolutionarily conserved master regulator of vascular development in vertebrates. Etv2 deficiency prevents the proper specification of the endothelial cell lineage, while its overexpression causes expansion of the endothelial cell lineage in the early embryo or in embryonic stem cells. We hypothesized that Etv2 alone is capable of transdifferentiating later somatic cells into endothelial cells. Using heat shock inducible Etv2 transgenic zebrafish, we demonstrate that Etv2 expression alone is sufficient to transdifferentiate fast skeletal muscle cells into functional blood vessels. Following heat treatment, fast skeletal muscle cells turn on vascular genes and repress muscle genes. Time-lapse imaging clearly shows that muscle cells turn on vascular gene expression, undergo dramatic morphological changes, and integrate into the existing vascular network. Lineage tracing and immunostaining confirm that fast skeletal muscle cells are the source of these newly generated vessels. Microangiography and observed blood flow demonstrated that this new vasculature is capable of supporting circulation. Using pharmacological, transgenic, and morpholino approaches, we further establish that the canonical Wnt pathway is important for induction of the transdifferentiation process, whereas the VEGF pathway provides a maturation signal for the endothelial fate. Additionally, overexpression of Etv2 in mammalian myoblast cells, but not in other cell types examined, induced expression of vascular genes. We have demonstrated in zebrafish that expression of Etv2 alone is sufficient to transdifferentiate fast skeletal muscle into functional endothelial cells in vivo. Given the evolutionarily conserved function of this transcription factor and the responsiveness of mammalian myoblasts to Etv2, it is likely that mammalian muscle cells will respond similarly.
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http://dx.doi.org/10.1371/journal.pbio.1001590DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3708712PMC
January 2014

A novel anti-tumor inhibitor identified by virtual screen with PLK1 structure and zebrafish assay.

PLoS One 2013 26;8(4):e53317. Epub 2013 Apr 26.

Shenzhen Graduate School of Peking University, Shenzhen, China.

Polo-like kinase 1 (PLK1), one of the key regulators of mitosis, is a target for cancer therapy due to its abnormally high activity in several tumors. Plk1 is highly conserved and shares a nearly identical 3-D structure between zebrafish and humans. The initial 10 mitoses of zebrafish embryonic cleavages occur every∼30 minutes, and therefore provide a rapid assay to evaluate mitosis inhibitors including those targeting Plk1. To increase efficiency and specificity, we first performed a computational virtual screen of∼60000 compounds against the human Plk1 3-D structure docked to both its kinase and Polo box domain. 370 candidates with the top free-energy scores were subjected to zebrafish assay and 3 were shown to inhibit cell division. Compared to general screen for compounds inhibiting zebrafish embryonic cleavage, computation increased the efficiency by 11 folds. One of the 3 compounds, named I2, was further demonstrated to effectively inhibit multiple tumor cell proliferation in vitro and PC3 prostate cancer growth in Xenograft mouse model in vivo. Furthermore, I2 inhibited Plk1 enzyme activity in a dose dependent manner. The IC50 values of I2 in these assays are compatible to those of ON-01910, a Plk1 inhibitor currently in Phase III clinic trials. Our studies demonstrate that zebrafish assays coupled with computational screening significantly improves the efficiency of identifying specific regulators of biological targets. The PLK1 inhibitor I2, and its analogs, may have potential in cancer therapeutics.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0053317PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3637257PMC
December 2013

[On the road to integration of theory and practice in education].

Tijdschr Diergeneeskd 2012 Oct;137(10):690-1

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October 2012

Identification of vascular and hematopoietic genes downstream of etsrp by deep sequencing in zebrafish.

PLoS One 2012 16;7(3):e31658. Epub 2012 Mar 16.

Department of Molecular, Cell and Developmental Biology, University of California Los Angeles, Los Angeles, California, United States of America.

The transcription factor etsrp/Er71/Etv2 is a master control gene for vasculogenesis in all species studied to date. It is also required for hematopoiesis in zebrafish and mice. Several novel genes expressed in vasculature have been identified through transcriptional profiling of zebrafish embryos overexpressing etsrp by microarrays. Here we re-examined this transcriptional profile by Illumina RNA-sequencing technology, revealing a substantially increased number of candidate genes regulated by etsrp. Expression studies of 50 selected candidate genes from this dataset resulted in the identification of 39 new genes that are expressed in vascular cells. Regulation of these genes by etsrp was confirmed by their ectopic induction in etsrp overexpressing and decreased expression in etsrp deficient embryos. Our studies demonstrate the effectiveness of the RNA-sequencing technology to identify biologically relevant genes in zebrfish and produced a comprehensive profile of genes previously unexplored in vascular endothelial cell biology.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0031658PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3306315PMC
August 2012

Etsrp/Etv2 is directly regulated by Foxc1a/b in the zebrafish angioblast.

Circ Res 2012 Jan 1;110(2):220-9. Epub 2011 Dec 1.

Department of Molecular, Cell, and Developmental Biology, University of California, Los Angeles, 621 Charles E Young Dr South, Los Angeles, CA 90095-1606, USA.

Rationale: Endothelial cells are developmentally derived from angioblasts specified in the mesodermal germ cell layer. The transcription factor etsrp/etv2 is at the top of the known genetic hierarchy for angioblast development. The transcriptional events that induce etsrp expression and angioblast specification are not well understood.

Objective: We generated etsrp:gfp transgenic zebrafish and used them to identify regulatory regions and transcription factors critical for etsrp expression and angioblast specification from mesoderm.

Methods And Results: To investigate the mechanisms that initiate angioblast cell transcription during embryogenesis, we have performed promoter analysis of the etsrp locus in zebrafish. We describe three enhancer elements sufficient for endothelial gene expression when place in front of a heterologous promoter. The deletion of all 3 regulatory regions led to a near complete loss of endothelial expression from the etsrp promoter. One of the enhancers, located 2.3 kb upstream of etsrp contains a consensus FOX binding site that binds Foxc1a and Foxc1b in vitro by EMSA and in vivo using ChIP. Combined knockdown of foxc1a/b, using morpholinos, led to a significant decrease in etsrp expression at early developmental stages as measured by quantitative reverse transcriptase-polymerase chain reaction and in situ hybridization. Decreased expression of primitive erythrocyte genes scl and gata1 was also observed, whereas pronephric gene pax2a was relatively normal in expression level and pattern.

Conclusions: These findings identify mesodermal foxc1a/b as a direct upstream regulator of etsrp in angioblasts. This establishes a new molecular link in the process of mesoderm specification into angioblast.
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http://dx.doi.org/10.1161/CIRCRESAHA.111.251298DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3457812PMC
January 2012

[Management and social responsibility highlighted].

Authors:
Marieke Veldman

Tijdschr Diergeneeskd 2010 Sep;135(18):685

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September 2010

[New Veterinary Medicine Masters starting].

Authors:
Marieke Veldman

Tijdschr Diergeneeskd 2010 Sep;135(18):684

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September 2010

[Farm animal veterinarian of the future is an independent advisor].

Authors:
Marieke Veldman

Tijdschr Diergeneeskd 2010 Apr;135(7):300

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April 2010

Tuba1a gene expression is regulated by KLF6/7 and is necessary for CNS development and regeneration in zebrafish.

Mol Cell Neurosci 2010 Apr 1;43(4):370-83. Epub 2010 Feb 1.

Neuroscience Program, University of Michigan, Biomedical Sciences Research Building, 109 Zina Pitcher Place, Ann Arbor, MI 48109, USA.

We report that knockdown of the alpha1 tubulin isoform Tuba1a, but not the highly related Tuba1b, dramatically impedes nervous system formation during development and RGC axon regeneration following optic nerve injury in adults. Within the tuba1a promoter, a G/C-rich element was identified that is necessary for tuba1a induction during RGC differentiation and optic axon regeneration. KLF6a and 7a, which we previously reported are essential for optic axon regeneration (Veldman et al., 2007), bind this G/C-rich element and transactivate the tuba1a promoter. In vivo knockdown of KLF6a and 7a attenuate regeneration-dependent activation of the endogenous tuba1a and p27 genes. These results suggest tuba1a expression is necessary for CNS development and regeneration and that KLF6a and 7a mediate their effects, at least in part, via transcriptional control of tuba1a promoter activity.
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http://dx.doi.org/10.1016/j.mcn.2010.01.004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2837137PMC
April 2010

[Veterinary Medicine Masters degree fits in the new veterinary education].

Authors:
Marieke Veldman

Tijdschr Diergeneeskd 2009 Sep;134(18):768-9

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September 2009

[How are the students at the ULP doing?].

Authors:
Marieke Veldman

Tijdschr Diergeneeskd 2009 Sep;134(18):767

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September 2009

[Birds and special animals in Europe under one umbrella].

Authors:
Mark Veldman

Tijdschr Diergeneeskd 2009 Jun;134(12):535

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June 2009

[Guarantees and education go together in the ULP].

Authors:
Marieke Veldman

Tijdschr Diergeneeskd 2009 Apr;134(7):306

Faculteit Diergeneeskunde.

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April 2009

Discovery and characterization of novel vascular and hematopoietic genes downstream of etsrp in zebrafish.

PLoS One 2009 24;4(3):e4994. Epub 2009 Mar 24.

Department of Molecular, Cell and Developmental Biology, University of California Los Angeles, Los Angeles, California, United States of America.

The transcription factor Etsrp is required for vasculogenesis and primitive myelopoiesis in zebrafish. When ectopically expressed, etsrp is sufficient to induce the expression of many vascular and myeloid genes in zebrafish. The mammalian homolog of etsrp, ER71/Etv2, is also essential for vascular and hematopoietic development. To identify genes downstream of etsrp, gain-of-function experiments were performed for etsrp in zebrafish embryos followed by transcription profile analysis by microarray. Subsequent in vivo expression studies resulted in the identification of fourteen genes with blood and/or vascular expression, six of these being completely novel. Regulation of these genes by etsrp was confirmed by ectopic induction in etsrp overexpressing embryos and decreased expression in etsrp deficient embryos. Additional functional analysis of two newly discovered genes, hapln1b and sh3gl3, demonstrates their importance in embryonic vascular development. The results described here identify a group of genes downstream of etsrp likely to be critical for vascular and/or myeloid development.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0004994PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2654924PMC
July 2009

[Modern education with the faculty veterinary medicine].

Authors:
Marieke Veldman

Tijdschr Diergeneeskd 2009 Feb;134(3):122-3

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February 2009

Percutaneous parathyroid ethanol ablation in patients with multiple endocrine neoplasia type 1.

AJR Am J Roentgenol 2008 Dec;191(6):1740-4

Department of Radiology, Mayo Clinic, 200 1st St., SW, Rochester, MN 55902, USA.

Objective: The objective of our study was to show the efficacy and safety of percutaneous ethanol ablation in managing recurrent primary hyperparathyroidism in patients with multiple endocrine neoplasia type 1 (MEN1) after subtotal parathyroidectomy.

Conclusion: Ethanol ablation is a viable alternative to reoperation for the management of recurrent primary hyperparathyroidism in patients with MEN1.
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http://dx.doi.org/10.2214/AJR.07.3431DOI Listing
December 2008

[Veterinarians in the media].

Authors:
Marieke Veldman

Tijdschr Diergeneeskd 2008 Jul 15-Aug 1;133(14-15):638-9

KNMVD.

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October 2008

Highly-restricted, cell-specific expression of the simian CMV-IE promoter in transgenic zebrafish with age and after heat shock.

Gene Expr Patterns 2009 Jan 6;9(1):54-64. Epub 2008 Aug 6.

Molecular and Behavioral Neuroscience Institute, Department of Biological Chemistry, University of Michigan, Ann Arbor, MI 48109-2200, USA.

Promoters with high levels of ubiquitous expression are of significant utility in the production of transgenic animals and cell lines. One such promoter is derived from the human cytomegalovirus immediate early (CMV-IE) gene. We sought to ascertain if the simian CMV-IE promoter (sCMV), used extensively in non-mammalian vertebrate research, also directs intense, widespread expression when stably introduced into zebrafish. Analysis of sCMV-driven expression revealed a temporal and spatial pattern not predicted by studies using the hCMV promoter in other transgenic animals or by observations of early F0 embryos expressing injected sCMV-reporter plasmids. Unexpectedly, in transgenic fish produced by both integration of linearized plasmid or Tol2-mediated transgenesis, sCMV promoter expression was generally observed in a small population of cells in telencephalon and spinal cord between days 2 and 7, and was thereafter confined to discrete regions of CNS that included the olfactory bulb, retina, cerebellum, spinal cord, and lateral line. In skeletal muscle, intense transgene expression was not observed until well into adulthood (>2-3 months post-fertilization). One final unexpected characteristic of the sCMV promoter in stable transgenic fish was tissue-specific responsiveness of the promoter to heat shock at both embryonic and adult stages. These data suggest that, in the context of stable transgenesis, the simian CMV-IE gene promoter responds differently to intracellular regulatory forces than other characterized CMV promoters.
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http://dx.doi.org/10.1016/j.gep.2008.07.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2650475PMC
January 2009

Zebrafish as a developmental model organism for pediatric research.

Pediatr Res 2008 Nov;64(5):470-6

Department of Molecular, Cellular, and Developmental Biology, University of California, Los Angeles, California 90095, USA.

Zebrafish has many advantages as a model of human pediatric research. Given the physical and ethical problems with performing experiments on human patients, biomedical research has focused on using model organisms to study biologic processes conserved between humans and lower vertebrates. The most common model organisms are small mammals, usually rats and mice. Although these models have significant advantages, they are also expensive to maintain, difficult to manipulate embryonically, and limited for large-scale genetic studies. The zebrafish model nicely complements these deficiencies in mammalian experimental models. The low cost, small size, and external development of zebrafish make it an excellent model for vertebrate development biology. Techniques for large-scale genome mutagenesis and gene mapping, transgenesis, protein overexpression or knockdown, cell transplantation and chimeric embryo analysis, and chemical screens have immeasurably increased the power of this model organism. It is now possible to rapidly determine the developmental function of a gene of interest in vivo, and then identify genetic and chemical modifiers of the processes involved. Discoveries made in zebrafish can be further validated in mammals. With novel technologies being regularly developed, the zebrafish is poised to significantly improve our understanding of vertebrate development under normal and pathologic conditions.
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http://dx.doi.org/10.1203/PDR.0b013e318186e609DOI Listing
November 2008

Gene expression analysis of zebrafish retinal ganglion cells during optic nerve regeneration identifies KLF6a and KLF7a as important regulators of axon regeneration.

Dev Biol 2007 Dec 22;312(2):596-612. Epub 2007 Sep 22.

Neuroscience Program, University of Michigan, 5045 Biomedical Sciences Research Building, 109 Zina Pitcher Place, Ann Arbor, MI 48109, USA.

Unlike mammals, teleost fish are able to mount an efficient and robust regenerative response following optic nerve injury. Although it is clear that changes in gene expression accompany axonal regeneration, the extent of this genomic response is not known. To identify genes involved in successful nerve regeneration, we analyzed gene expression in zebrafish retinal ganglion cells (RGCs) regenerating their axons following optic nerve injury. Microarray analysis of RNA isolated by laser capture microdissection from uninjured and 3-day post-optic nerve injured RGCs identified 347 up-regulated and 29 down-regulated genes. Quantitative RT-PCR and in situ hybridization were used to verify the change in expression of 19 genes in this set. Gene ontological analysis of the data set suggests regenerating neurons up-regulate genes associated with RGC development. However, not all regeneration-associated genes are expressed in differentiating RGCs indicating the regeneration is not simply a recapitulation of development. Knockdown of six highly induced regeneration-associated genes identified two, KLF6a and KLF7a, that together were necessary for robust RGC axon re-growth. These results implicate KLF6a and KLF7a as important mediators of optic nerve regeneration and suggest that not all induced genes are essential to mount a regenerative response.
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http://dx.doi.org/10.1016/j.ydbio.2007.09.019DOI Listing
December 2007

Characterization of a muscle-specific enhancer in human MuSK promoter reveals the essential role of myogenin in controlling activity-dependent gene regulation.

J Biol Chem 2006 Feb 18;281(7):3943-53. Epub 2005 Dec 18.

Molecular and Behavior Neuroscience Institute and Department of Biological Chemistry, University of Michigan, Ann Arbor, 48109, USA.

Neuromuscular synaptogenesis is initiated by the release of agrin from motor neurons and the activation of the receptor tyrosine kinase, MuSK, in the postsynaptic membrane. MuSK gene expression is regulated by nerve-derived agrin and muscle activity. Agrin stimulates synapse-specific MuSK gene expression by activating GABP(alphabeta) transcription factors in endplate-associated myonuclei. In contrast, the mechanism by which muscle activity regulates MuSK gene expression is not known. We report on a 60-bp MuSK enhancer that confers promoter regulation by muscle differentiation, changes in intracellular calcium, and muscle activity. Within this enhancer, we identified a single E-box that is essential for this regulation. This E-box binds myogenin, and we showed that myogenin is necessary for not only MuSK but also nAChR gene regulation by muscle activity. Surprisingly, the same E-box functions in vivo to mediate muscle-specific and differentiation-dependent gene induction in zebrafish, suggesting an evolutionary conserved mechanism of regulation of synaptic protein gene expression.
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http://dx.doi.org/10.1074/jbc.M511317200DOI Listing
February 2006

[Dad, the rabbits have grown up!].

Authors:
Marieke Veldman

Tijdschr Diergeneeskd 2005 Oct;130(20):647-8

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October 2005

[Oxygen for the Dutch veterinarian].

Authors:
M Veldman

Tijdschr Diergeneeskd 2004 Jul 15-Aug 1;129(14-15):499-500

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October 2004

Plasma MMP-2 and MMP-9 and their inhibitors TIMP-1 and TIMP-2 during human orthotopic liver transplantation. The effect of aprotinin and the relation to ischemia/reperfusion injury.

Thromb Haemost 2004 Mar;91(3):506-13

Department of Gastroenterology and Hepatology, Leiden University Medical Center, C4-P, PO. Box 9600, 2300 RC Leiden, The Netherlands.

Uncontrolled activation of matrix metalloproteinases (MMPs) can result in tissue injury and inflammation, yet little is known about the activation of MMPs during orthotopic liver transplantation (OLT). OLT is associated with increased fibrinolytic activity due to elevated plasmin generation. The serine-protease plasmin not only causes degradation of fibrin clots but is also thought, amongst others, to play a role in the activation of some matrix metalloproteinases. We therefore studied the evolution of MMP-2 and -9 plasma concentrations during OLT and the effect of serine-protease inhibition by aprotinin on the level and activation of these MMPs. In a group of 24 patients who participated in a randomized, double-blind, placebo-controlled study we determined serial MMP-2 and MMP-9 plasma levels during transplantation using ELISA (total MMP), activity assays (activatable MMP) and zymography. In addition, the MMP-inhibitors TIMP-1 and TIMP-2 were assessed by ELISA. The putative regulating factors tumor necrosis factor alpha (TNF-alpha) and tissue-type plasminogen activator (t-PA) were assessed as well. Patients were administered high-dose aprotinin, regular-dose aprotinin or placebo during surgery. Plasma TIMP-1, TIMP-2 and MMP-2 level gradually decreased during transplantation. Approximately two-thirds of total MMP-2 appeared to be in its activatable proMMP form. No release of MMP-2 from the graft could be detected. In contrast, plasma levels of MMP-9 increased sharply during the anhepatic and postreperfusion periods. Peak MMP-9 levels of about eight times above baseline were found at 30 minutes after reperfusion. Most MMP-9 appeared to be in its active/inhibitor-complexed form. No significant differences were observed between the three treatment groups. However, in patients with more severe ischemia/reperfusion (I/R) injury the MMP-9 concentration, particularly of the active/inhibitor-complexed form, remained high at 120 minutes postreperfusion compared to patients with no or mild I/R injury. The decrease in plasma levels of MMP-2, TIMP-1 and TIMP-2 during OLT occurred irrespective of the severity of the I/R injury. There was a significant correlation between MMP-9 and t-PA levels, but not with TNF-alpha. In conclusion, OLT is associated with a sharp increase of MMP-9 during the anhepatic and postreperfusion periods, which coincided with the changes in t-PA. MMP-2, TIMP-1 and TIMP-2 gradually decreased during OLT. The composition of these MMPs was not altered by the use of aprotinin, suggesting that serine-protease/plasmin-independent pathways are responsible for MMP regulation during OLT. In addition, only MMP-9 seems to be involved in I/R injury during human liver transplantation.
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http://dx.doi.org/10.1160/TH03-05-0272DOI Listing
March 2004

Chemical and sensory evaluation of crude oil extracted from herring byproducts from different processing operations.

J Agric Food Chem 2003 Mar;51(7):1897-903

Netherlands Institute for Fisheries Research (RIVO), P.O. Box 68, 1970 AB IJmuiden, The Netherlands.

Fish oils extracted from marinated herring (frozen and unfrozen) byproducts and maatjes herring byproducts were evaluated on their chemical and sensory properties. The obtained crude oils had very low content of copper (<0.1 mg/kg oil), and iron values were 0.8, 0.1, and 0.03 mg/kg oil, respectively, for oil from maatjes and frozen and fresh byproducts. For the maatjes oil, a much lower value was found for alpha-tocopherol compared to the other oils. Storage stability results showed that the oils behave differently. Secondary oxidation products were measured for fresh oil, while for the maatjes and frozen byproducts' oil, tertiary oxidation products were detected. Over storage time, the maatjes and frozen byproducts' oils became more intense in odor, correlating positively at the end with sensory attributes of train-oil, acidic, marine and fishy. The best correlation between sensory and chemical analyses was found for FFA and fishy off-odor (r = 0.781).
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http://dx.doi.org/10.1021/jf020684pDOI Listing
March 2003

Improved early graft survival in patients receiving aprotinin during orthotopic liver transplantation.

Transplant Proc 2001 Feb-Mar;33(1-2):1345-6

Department of Surgery, Leiden University Medical Center, Leiden, The Netherlands.

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http://dx.doi.org/10.1016/s0041-1345(00)02503-3DOI Listing
June 2001

TS+OCD-like neuropotentiated mice are supersensitive to seizure induction.

Neuroreport 2000 Jul;11(10):2335-8

Department of Pharmacology, University of Minnesota, Minneapolis 55455, USA.

Seizures can be induced by systemic dopamine D1 receptor agonists or by cortical-limbic neurostimulation non-selectively. Seizures are also often associated with tics and compulsions, which likewise involve cortical-limbic hyperactivity. To determine if selective potentiation of cortical-limbic D1 receptor-expressing (D1+) neurons increases seizure susceptibility, we administered pentylenetetrazole (PTZ) to mice that express a neuropotentiating transgene only in a glutamatergic, cortical-limbic subset of D1+ neurons (D1CT-7 line). These mice exhibited increased PTZ-dependent seizure incidence, onset rate and intensity. Because D1CT-7 mice also exhibit tic+compulsion-like behaviors, this implies that glutamatergic hyperactivity induced by cortical-limbic D1+ neuropotentiation facilitates not only epilepsy but also tics and compulsions. This suggests a dopamine-regulated glutamatergic basis for all three states and may explain why they often co-exist in humans.
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http://dx.doi.org/10.1097/00001756-200007140-00053DOI Listing
July 2000

Anxiety in a transgenic mouse model of cortical-limbic neuro-potentiated compulsive behavior.

Behav Pharmacol 1999 Sep;10(5):435-43

Department of Pharmacology, University of Minnesota, Minneapolis 55455, USA.

Anxiety and amygdalar stimulation may induce or exacerbate compulsions triggered by cortical-limbic hyperactivity, as in human obsessive-compulsive disorder (OCD). We previously created transgenic mice that exhibit OCD-like biting, movement and behavioral perseverance abnormalities. These behaviors are caused by expression of a neuro-potentiating cholera toxin (CT) transgene in dopamine D1 receptor-expressing (D1+) neurons within the amygdalar intercalated nucleus (ICN) and within cortical areas that project to orbitofrontal cortex and striatum. Here we tested whether anxiety and increased amygdalar stimulation may play a role in eliciting or exacerbating such behaviors. D1CT mice exhibited increased thigmotaxis (tendency of mice to remain along the perimeter of open areas) in the open field assay, and increased latency to first transit and reduced transit number in the light-dark assay. These studies indicate that the D1CT mice exhibit a significant increase in behavioral indicators of anxiety. Furthermore, yohimbine, a drug that induces both amygdalar stimulation and behavioral indicators of anxiety, exacerbated abnormal leaping in D1CT mice but failed to exacerbate their abnormal behavioral perseverance. These data suggest that chronic potentiation of D1+ neurons in the amygdalar ICN increases anxiety and facilitates particular compulsive behaviors.
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http://dx.doi.org/10.1097/00008877-199909000-00001DOI Listing
September 1999
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