Letter from Cornelia Maaike van Malsen Vander Luister to Her Parents, Brothers, and Sister

A letter of Cornelia Maaike van Malsen Vande Luister [she had been married to Jannis Vande Luister on September 11 by Albertus C. Van Raalte] to her parents, brothers, and sister, about many family matters because she had heard from her parents on November 12. She then gave a report on life in the Van Raalte family: I am still in the household of Rev. Van Raalte but am going to my own house this week. The pastor and his wife are my dear friends; we have very much in common. The Lord grant that I may find grace in the in the eyes of the people. All three of us (the minister, his wife, and I) are writing to the Netherlands. It is nine o\u27clock in the evening. The dear little ones are in bed. The two smallest—Christina, a dear little girl of about two and Dirk, a lad of four, call me aunt ; they are all fond of me. I will have the youngest for fourteen days as soon as he is weaned. Benjamin is seven; then comes Mina, nine; and Albertus, who is eleven years old. Arie, you should see how neatly those boys can chop wood. They all have little axes, even little Dirk... We have already been with this good family for three months... During the winter months our English teacher comes to instruct both the children and the adults, especially in English. The minister and his wife pray constantly for a God-fearing teacher... (Van Raalte) has so much to do that I often feel sorry for him. She is also urging her parents to come to America and gives them advice about the trip and what they need to take.https://digitalcommons.hope.edu/vrp_1840s/1132/thumbnail.jp

Relational Model Conflicts in Knowledge Sharing Behavior

The distributed nature of organizational knowledge makes that knowledge sharing an important factor for unlocking its potential value. In practice, however, people may have different motivations for not sharing knowledge with colleagues, which in part may be due to the relational context. In this paper, we adopt Fiske’s Relational Model Theory to investigate relational dynamics in knowledge sharing behavior. Our objective is to gain insight into how relational model conflicts affect knowledge sharing in organizations. A series of experiments have been conducted, in which the consequences of relational model conflicts for the willingness to share knowledge are evaluated. Each experiment contained four scenarios reflecting different relational models. Participants were faced with different scenarios reflecting particular relational models, and a fictitious other colleague who behaved according to a conflicting relational model. Our analysis shows that the recognition of relational model conflicts strongly depends on the relational models involved. The extent of recognition seems to be related with the nature of the exchange relationships involved in the conflict. For instance, the relational model conflict was more acutely felt by a communal sharing participant facing a market pricing colleague, than by the same participant dealing with an authority ranking response. Likewise, we find that the impact of relational model conflicts on the willingness to share knowledge depends on the relational models involved. Specifically, it appears that market pricing responses have a negative influence on participants’ willingness to share, while communal sharing responses generally have positive effects. Our research serves as a starting point for other studies aiming at a deeper understanding of the dynamics of knowledge sharing behavior of employees and for solving conflicts at work

Hippocampal Gene Expression Analysis Highlights Ly6a/Sca-1 as Candidate Gene for Previously Mapped Novelty Induced Behaviors in Mice

In this study, we show that the covariance between behavior and gene expression in the brain can help further unravel the determinants of neurobehavioral traits. Previously, a QTL for novelty induced motor activity levels was identified on murine chromosome 15 using consomic strains. With the goal of narrowing down the linked region and possibly identifying the gene underlying the quantitative trait, gene expression data from this F2-population was collected and used for expression QTL analysis. While genetic variation in these mice was limited to chromosome 15, eQTL analysis of gene expression showed strong cis-effects as well as trans-effects elsewhere in the genome. Using weighted gene co-expression network analysis, we were able to identify modules of co-expressed genes related to novelty induced motor activity levels. In eQTL analyses, the expression of Ly6a (a.k.a. Sca-1) was found to be cis-regulated by chromosome 15. Ly6a also surfaced in a group of genes resulting from the network analysis that was correlated with behavior. Behavioral analysis of Ly6a knock-out mice revealed reduced novelty induced motor activity levels when compared to wild type controls, confirming functional importance of Ly6a in this behavior, possibly through regulating other genes in a pathway. This study shows that gene expression profiling can be used to narrow down a previously identified behavioral QTL in mice, providing support for Ly6a as a candidate gene for functional involvement in novelty responsiveness

Family-based association analysis to finemap bipolar linkage peak on chromosome 8q24 using 2,500 genotyped SNPs and 15,000 imputed SNPs

Zhang P, Xiang N, Chen Y, Śliwerska E, McInnis MG, Burmeister M, Zöllner S. Family-based association analysis to finemap bipolar linkage peak on chromosome 8q24 using 2,500 genotyped SNPs and 15,000 imputed SNPs. Bipolar Disord 2010: 12: 786–792. © 2010 The Authors. Journal compilation © 2010 John Wiley & Sons A/S.Multiple linkage and association studies have suggested chromosome 8q24 as a promising candidate region for bipolar disorder (BP). We performed a detailed association analysis assessing the contribution of common genetic variation in this region to the risk of BP.We analyzed 2,756 single nucleotide polymorphism (SNP) markers in the chromosome 8q24 region of 3,512 individuals from 737 families. In addition, we extended genotype imputation methods to family-based data and imputed 22,725 HapMap SNPs in the same region on 8q24. We applied a family-based method to test 15,552 high-quality genotyped or imputed SNPs for association with BP.Our association analysis identified the most significant marker (p = 4.80 × 10 −5 ), near the gene encoding potassium voltage-gated channel KQT-like protein ( KCNQ3 ). Other marginally significant markers were located near adenylate cyclase 8 ( ADCY8 ) and ST3 beta-galactoside alpha-2,3-sialyltransferase 1 ( ST3GAL1 ).We developed an approach to apply MACH imputation to family-based data, which can increase the power to detect association signals. Our association results showed suggestive evidence of association of BP with loci near KCNQ3 , ADCY8 , and ST3GAL1 . Consistent with genes identified by genome-wide association studies for BP, our results suggest the involvement of ion channelopathy in BP pathogenesis. However, common variants are insufficient to explain linkage findings in 8q24; other genetic variation should be explored.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/79302/1/j.1399-5618.2010.00883.x.pd

Partial change in EphA4 knockout mouse phenotype: Loss of diminished GFAP upregulation following spinal cord injury

In a previous study we found that the EphA4 receptor inhibits regeneration following spinal cord injury by blocking regrowth of axons and regulation of astrocyte reactivity. In our original studies using EphA4 null mice [Goldshmit et al., J. Neurosci., 2004] we found attenuated astrocyte reactivity following spinal cord injury. Several other studies have now supported the role of EphA4 in regulating neural regeneration but a recent study [Herrmann et al., Exp. Neurol., 2010] did not find an effect of EphA4 on astrocyte reactivity. Re-examination of astrocytic gliosis following injury in our current cohort of EphA4 null mice revealed that they no longer showed attenuation of astrocyte reactivity, however other EphA4 null mouse phenotypes, such as decreased size of the dorsal funiculus were unaltered. We hypothesised that long-term breeding on the C57Bl/6 background may influence the EphA4-mediated astrocyte phenotype and compared astrocytic gliosis at 4 days following spinal cord injury in wildtype and EphA4 null mice on the C57Bl/6 background and backcrossed C57Bl/6×129Sv(F2) mice, as well as wildtype 129Sv mice. 129Sv mice had increased GFAP expression and increased numbers of reactive GFAP astrocytes compared to C57Bl/6 mice. There was no significant effect of EphA4 deletion on GFAP expression in C57Bl/6 mice or the F2 crosses other than a moderately decreased number of EphA4 null astrocytes in C57Bl/6 mice using one of two antibodies. Therefore, there has been an apparent change in EphA4-mediated astroglial phenotype associated with long term breeding of the EphA4 colony but it does not appear to be influenced by background mouse strain

Bioinformatics tools and database resources for systems genetics analysis in mice—a short review and an evaluation of future needs

During a meeting of the SYSGENET working group ‘Bioinformatics’, currently available software tools and databases for systems genetics in mice were reviewed and the needs for future developments discussed. The group evaluated interoperability and performed initial feasibility studies. To aid future compatibility of software and exchange of already developed software modules, a strong recommendation was made by the group to integrate HAPPY and R/qtl analysis toolboxes, GeneNetwork and XGAP database platforms, and TIQS and xQTL processing platforms. R should be used as the principal computer language for QTL data analysis in all platforms and a ‘cloud’ should be used for software dissemination to the community. Furthermore, the working group recommended that all data models and software source code should be made visible in public repositories to allow a coordinated effort on the use of common data structures and file formats

Identifying Human Disease Genes through Cross-Species Gene Mapping of Evolutionary Conserved Processes

Understanding complex networks that modulate development in humans is hampered by genetic and phenotypic heterogeneity within and between populations. Here we present a method that exploits natural variation in highly diverse mouse genetic reference panels in which genetic and environmental factors can be tightly controlled. The aim of our study is to test a cross-species genetic mapping strategy, which compares data of gene mapping in human patients with functional data obtained by QTL mapping in recombinant inbred mouse strains in order to prioritize human disease candidate genes.We exploit evolutionary conservation of developmental phenotypes to discover gene variants that influence brain development in humans. We studied corpus callosum volume in a recombinant inbred mouse panel (C57BL/6J×DBA/2J, BXD strains) using high-field strength MRI technology. We aligned mouse mapping results for this neuro-anatomical phenotype with genetic data from patients with abnormal corpus callosum (ACC) development.).This approach that exploits highly diverse mouse strains provides an efficient and effective translational bridge to study the etiology of human developmental disorders, such as autism and schizophrenia