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Search Results: 1 - 10 of 297442 matches for " Hermien J Elgersma "
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Disrupting the rhythm of depression: design and protocol of a randomized controlled trial on preventing relapse using brief cognitive therapy with or without antidepressants
Claudi LH Bockting, Hermien J Elgersma, Gerard D van Rijsbergen, Peter de Jonge, Johan Ormel, Erik Buskens, A Dennis Stant, Peter J de Jong, Frenk PML Peeters, Marcus JH Huibers, Arnoud Arntz, Peter Muris, Willem A Nolen, Aart H Schene, Steven D Hollon
BMC Psychiatry , 2011, DOI: 10.1186/1471-244x-11-8
Abstract: Therefore, we will compare the effectiveness and cost-effectiveness of brief CT while tapering AD to maintenance AD and the combination of CT with maintenance AD. In addition, we examine whether the prophylactic effect of CT was due to CT tackling illness related risk factors for recurrence such as residual symptoms or to its efficacy to modify presumed vulnerability factors of recurrence (e.g. rigid explicit and/or implicit dysfunctional attitudes). This is a multicenter RCT comparing the above treatment scenarios. Remitted patients on AD with at least two previous depressive episodes in the past five years (n = 276) will be recruited. The primary outcome is time related proportion of depression relapse/recurrence during minimal 15 months using DSM-IV-R criteria as assessed by the Structural Clinical Interview for Depression. Secondary outcome: economic evaluation (using a societal perspective) and number, duration and severity of relapses/recurrences.This will be the first trial to investigate whether CT is effective in preventing relapse to depression in recurrent depression while tapering antidepressant treatment compared to antidepressant treatment alone and the combination of both. In addition, we explore explicit and implicit mediators of CT.Netherlands Trial Register (NTR): NTR1907Major depressive disorder (MDD) is projected to rank second on a list of 15 major diseases in terms of burden of disease in 2030 [1]. The major contribution of MDD to disability and health care costs is largely due to its highly recurrent nature [2,3]. Accordingly, efforts to reduce the disabling effects of depression should shift to preventing recurrences, especially in patients at high risk of recurrence. Several international guidelines (e.g., [4,5]) report that patients remitted from prior depressive episodes belong to such high risk groups. The preventive strategy globally suggested, i.e. continuation of antidepressants (AD) for years, is certainly not in line with the fact th
Rekenaargeletterdheid vir voorgraadse studente; ‘n onderrigprogram
Marlene J Viljoen,Hermien Johannes
Health SA Gesondheid , 1998, DOI: 10.4102/hsag.v4i3.361
Abstract: The need for basic computer skills as well as information gathering and information processing skills are becoming more important at the School of Nursing, UOFS. Opsomming Basiese rekenaarvaardighede sowel as inligtingverkrygings- en inligtingverwerkingsvaardighede word toenemend 'n behoefte aan die Skool vir Verpleegkunde aan die UOVS. *Please note: This is a reduced version of the abstract. Please refer to PDF for full text.
α-Calcium Calmodulin Kinase II Modulates the Temporal Structure of Hippocampal Bursting Patterns
Jeiwon Cho, Rushi Bhatt, Ype Elgersma, Alcino J. Silva
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0031649
Abstract: The alpha calcium calmodulin kinase II (α-CaMKII) is known to play a key role in CA1/CA3 synaptic plasticity, hippocampal place cell stability and spatial learning. Additionally, there is evidence from hippocampal electrophysiological slice studies that this kinase has a role in regulating ion channels that control neuronal excitability. Here, we report in vivo single unit studies, with α-CaMKII mutant mice, in which threonine 305 was replaced with an aspartate (α-CaMKIIT305D mutants), that indicate that this kinase modulates spike patterns in hippocampal pyramidal neurons. Previous studies showed that α-CaMKIIT305D mutants have abnormalities in both hippocampal LTP and hippocampal-dependent learning. We found that besides decreased place cell stability, which could be caused by their LTP impairments, the hippocampal CA1 spike patterns of α-CaMKIIT305D mutants were profoundly abnormal. Although overall firing rate, and overall burst frequency were not significantly altered in these mutants, inter-burst intervals, mean number of intra-burst spikes, ratio of intra-burst spikes to total spikes, and mean intra-burst intervals were significantly altered. In particular, the intra burst intervals of place cells in α-CaMKIIT305D mutants showed higher variability than controls. These results provide in vivo evidence that besides its well-known function in synaptic plasticity, α-CaMKII, and in particular its inhibitory phosphorylation at threonine 305, also have a role in shaping the temporal structure of hippocampal burst patterns. These results suggest that some of the molecular processes involved in acquiring information may also shape the patterns used to encode this information.
Ontwikkeling na multimediagesteunde verpleegonderwys
Hermien Johannes
Health SA Gesondheid , 1998, DOI: 10.4102/hsag.v3i2.351
Abstract: Today's rapidly changing world creates high educational demands on nursing education and the nursing profession. Opsomming Die vinnig veranderende hedendaagse wereld stel hoe onderrigeise aan verpleegonderwys en die verpleegprofessie. *Please note: This is a reduced version of the abstract. Please refer to PDF for full text.
Breast density as indicator for the use of mammography or MRI to screen women with familial risk for breast cancer (FaMRIsc): a multicentre randomized controlled trial
Saadatmand Sepideh,Rutgers Emiel J T,Tollenaar RobAEM,Zonderland Hermien M
BMC Cancer , 2012, DOI: 10.1186/1471-2407-12-440
Abstract: Background To reduce mortality, women with a family history of breast cancer often start mammography screening at a younger age than the general population. Breast density is high in over 50% of women younger than 50 years. With high breast density, breast cancer incidence increases, but sensitivity of mammography decreases. Therefore, mammography might not be the optimal method for breast cancer screening in young women. Adding MRI increases sensitivity, but also the risk of false-positive results. The limitation of all previous MRI screening studies is that they do not contain a comparison group; all participants received both MRI and mammography. Therefore, we cannot empirically assess in which stage tumours would have been detected by either test. The aim of the Familial MRI Screening Study (FaMRIsc) is to compare the efficacy of MRI screening to mammography for women with a familial risk. Furthermore, we will assess the influence of breast density. Methods/Design This Dutch multicentre, randomized controlled trial, with balanced randomisation (1:1) has a parallel grouped design. Women with a cumulative lifetime risk for breast cancer due to their family history of ≥20%, aged 30–55 years are eligible. Identified BRCA1/2 mutation carriers or women with 50% risk of carrying a mutation are excluded. Group 1 receives yearly mammography and clinical breast examination (n = 1000), and group 2 yearly MRI and clinical breast examination, and mammography biennially (n = 1000). Primary endpoints are the number and stage of the detected breast cancers in each arm. Secondary endpoints are the number of false-positive results in both screening arms. Furthermore, sensitivity and positive predictive value of both screening strategies will be assessed. Cost-effectiveness of both strategies will be assessed. Analyses will also be performed with mammographic density as stratification factor. Discussion Personalized breast cancer screening might optimize mortality reduction with less over diagnosis. Breast density may be a key discriminator for selecting the optimal screening strategy for women < 55 years with familial breast cancer risk; mammography or MRI. These issues are addressed in the FaMRIsc study including high risk women due to a familial predisposition. Trial registration Netherland Trial Register NTR2789
李锋瑞, A. Elgersma
植物生态学报 植物生态学报 , 1998,
31P MR Spectroscopy and Computational Modeling Identify a Direct Relation between Pi Content of an Alkaline Compartment in Resting Muscle and Phosphocreatine Resynthesis Kinetics in Active Muscle in Humans
Joep W. M. van Oorschot, Joep P. J. Schmitz, Andrew Webb, Klaas Nicolay, Jeroen A. L. Jeneson, Hermien E. Kan
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0076628
Abstract: The assessment of mitochondrial properties in skeletal muscle is important in clinical research, for instance in the study of diabetes. The gold standard to measure mitochondrial capacity non-invasively is the phosphocreatine (PCr) recovery rate after exercise, measured by 31P Magnetic Resonance spectroscopy (31P MRS). Here, we sought to expand the evidence base for an alternative method to assess mitochondrial properties which uses 31P MRS measurement of the Pi content of an alkaline compartment attributed to mitochondria (Pi2; as opposed to cytosolic Pi (Pi1)) in resting muscle at high magnetic field. Specifically, the PCr recovery rate in human quadriceps muscle was compared with the signal intensity of the Pi2 peak in subjects with varying mitochondrial content of the quadriceps muscle as a result of athletic training, and the results were entered into a mechanistic computational model of mitochondrial metabolism in muscle to test if the empirical relation between Pi2/Pi1 ratio and the PCr recovery was consistent with theory. Localized 31P spectra were obtained at 7T from resting vastus lateralis muscle to measure the intensity of the Pi2 peak. In the endurance trained athletes a Pi2/Pi1 ratio of 0.07 ± 0.01 was found, compared to a significantly lower (p<0.05) Pi2/Pi1 ratio of 0.03 ± 0.01 in the normally active group. Next, PCr recovery kinetics after in magnet bicycle exercise were measured at 1.5T. For the endurance trained athletes, a time constant τPCr 12 ± 3 s was found, compared to 24 ± 5s in normally active subjects. Without any parameter optimization the computational model prediction matched the experimental data well (r2 of 0.75). Taken together, these results suggest that the Pi2 resonance in resting human skeletal muscle observed at 7T provides a quantitative MR-based functional measure of mitochondrial density.
Functional Gene-Expression Analysis Shows Involvement of Schizophrenia-Relevant Pathways in Patients with 22q11 Deletion Syndrome
Nico J. M. van Beveren, Lianne C. Krab, Sigrid Swagemakers, Gabriella Buitendijk, Erik Boot, Peter van der Spek, Ype Elgersma, Therese A. M. J. van Amelsvoort
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0033473
Abstract: 22q11 Deletion Syndrome (22q11DS) is associated with dysmorphology and a high prevalence of schizophrenia-like symptoms. Several genes located on chromosome 22q11 have been linked to schizophrenia. The deletion is thought to disrupt the expression of multiple genes involved in maturation and development of neurons and neuronal circuits, and neurotransmission. We investigated whole-genome gene expression of Peripheral Blood Mononuclear Cells (PBMC's) of 8 22q11DS patients and 8 age- and gender-matched controls, to (1) investigate the expression levels of 22q11 genes and (2) to investigate whether 22q11 genes participate in functional genetic networks relevant to schizophrenia. Functional relationships between genes differentially expressed in patients (as identified by Locally Adaptive Statistical procedure (LAP) or satisfying p<0.05 and fold-change >1.5) were investigated with the Ingenuity Pathways Analysis (IPA). 14 samples (7 patients, 7 controls) passed quality controls. LAP identified 29 deregulated genes. Pathway analysis showed 262 transcripts differentially expressed between patients and controls. Functional pathways most disturbed were cell death, cell morphology, cellular assembly and organization, and cell-to-cell signaling. In addition, 10 canonical pathways were identified, among which the signal pathways for Natural Killer-cells, neurotrophin/Trk, neuregulin, axonal guidance, and Huntington's disease. Our findings support the use of 22q11DS as a research model for schizophrenia. We identified decreased expression of several genes (among which COMT, Ufd1L, PCQAP, and GNB1L) previously linked to schizophrenia as well as involvement of signaling pathways relevant to schizophrenia, of which Neurotrophin/Trk and neuregulin signaling seems to be especially notable.
Mammalian Target of Rapamycin Complex I (mTORC1) Activity in Ras Homologue Enriched in Brain (Rheb)-Deficient Mouse Embryonic Fibroblasts
Marlous J. Groenewoud, Susan M. I. Goorden, Jorien Kassies, Wendy Pellis-van Berkel, Richard F. Lamb, Ype Elgersma, Fried J. T. Zwartkruis
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0081649
Abstract: The Ras-like GTPase Rheb has been identified as a crucial activator of mTORC1. Activation most likely requires a direct interaction between Rheb and mTOR, but the exact mechanism remains unclear. Using a panel of Rheb-deficient mouse embryonic fibroblasts (MEFs), we show that Rheb is indeed essential for the rapid increase of mTORC1 activity following stimulation with insulin or amino acids. However, mTORC1 activity is less severely reduced in Rheb-deficient MEFs in the continuous presence of serum or upon stimulation with serum. This remaining mTORC1 activity is blocked by depleting the cells for amino acids or imposing energy stress. In addition, MEK inhibitors and the RSK-inhibitor BI-D1870 interfere in mTORC1 activity, suggesting that RSK acts as a bypass for Rheb in activating mTORC1. Finally, we show that this rapamycin-sensitive, Rheb-independent mTORC1 activity is important for cell cycle progression. In conclusion, whereas rapid adaptation in mTORC1 activity requires Rheb, a second Rheb-independent activation mechanism exists that contributes to cell cycle progression.
Marked Reduction of AKT1 Expression and Deregulation of AKT1-Associated Pathways in Peripheral Blood Mononuclear Cells of Schizophrenia Patients
Nico J. M. van Beveren, Gabrielle H. S. Buitendijk, Sigrid Swagemakers, Lianne C. Krab, Christian R?der, Lieuwe de Haan, Peter van der Spek, Ype Elgersma
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0032618
Abstract: Background Recent studies have suggested that deregulated AKT1 signaling is associated with schizophrenia. We hypothesized that if this is indeed the case, we should observe both decreased AKT1 expression as well as deregulation of AKT1 regulated pathways in Peripheral Blood Mononuclear Cells (PBMCs) of schizophrenia patients. Objectives To examine PBMC expression levels of AKT1 in schizophrenia patients versus controls, and to examine whether functional biological processes in which AKT1 plays an important role are deregulated in schizophrenia patients. Methods/Results A case-control study, investigating whole-genome PBMC gene expression in male, recent onset (<5 years) schizophrenia patients (N = 41) as compared to controls (N = 29). Genes, differentially expressed between patients and controls were identified using ANOVA with Benjamini-Hochberg correction (false discovery rate (FDR) = 0.05). Functional aspects of the deregulated set of genes were investigated with the Ingenuity Pathway Analysis (IPA) Software Tool. We found significantly decreased PBMC expression of AKT1 (p<0.001, t = ?4.25) in the patients. AKT1 expression was decreased in antipsychotic-free or -naive patients (N = 11), in florid psychotic (N = 20) and in remitted (N = 21) patients. A total of 1224 genes were differentially expressed between patients and controls (FDR = 0.05). Functional analysis of the entire deregulated gene set indicated deregulated canonical pathways involved in a large number of cellular processes: immune system, cell adhesion and neuronal guidance, neurotrophins and (neural) growth factors, oxidative stress and glucose metabolism, and apoptosis and cell-cycle regulation. Many of these processes are associated with AKT1. Conclusions We show significantly decreased PBMC gene expression of AKT1 in male, recent-onset schizophrenia patients. Our observations suggest that decreased PBMC AKT1 expression is a stable trait in recent onset, male schizophrenia patients. We identified several AKT related cellular processes which are potentially affected in these patients, a majority of which play a prominent role in current schizophrenia hypotheses.
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