Development and Evaluation of a Parenting Resilience Elements Questionnaire (PREQ) Measuring Resiliency in Rearing Children with Developmental Disorders

We developed a parenting resilience elements questionnaire (PREQ) measuring the degree to which mothers possess elements that aid in adapting to challenges and difficulties related to children with developmental disorders (DD). A total of 424 parents of children with DD were recruited from five medical institutes. Psychometric properties of PREQ were evaluated using data of 363 mothers of children with DD. Furthermore, multiple regression analysis was performed, predicting depressive symptoms and parenting behavior with PREQ subscales, a general health questionnaire, and the total difficulties score of a strength and difficulties questionnaire. Factor analysis revealed three reliable factors: “knowledge of the child’s characteristics,” “perceived social supports,” and “positive perceptions of parenting.” Moreover, multiple regression analysis showed that “knowledge of the child’s characteristics” was associated with parenting behavior, whereas “perceived social supports” predicted depressive symptoms; “positive perceptions of parenting” influenced both parenting behavior and depressive symptoms. These findings indicated that the PREQ may be used as a scale measuring resiliency in mothers of children with DD and is useful for evaluating their parenting ability in clinical interventions.     

Importance of mitochondrial dysfunction in oxidative stress response: A comparative study of gene expression profiles

Mitochondria are considered to play an important role in oxidative stress response since they are a source of reactive oxygen species and are also targeted by these species. This study examined the mitochondrial conditions in cells of epithelial origin that were exposed to H(2)O(2) and found a decline in the membrane potential along with a specific loss of UQCRC1, a sub-unit of complex III, suggesting that mitochondrial dysfunction occurs upon exposure to oxidative stress. This observation led to the hypothesis that certain cellular responses to oxidative stress occurred because of mitochondrial dysfunction. When mitochondria-less (pseudo ρ0) cells were examined as a model of mitochondrial dysfunction, striking similarities were found in their cellular responses compared with those found in cells exposed to oxidative stress, including changes in gene expression and gelatinolytic enzyme activities, thus suggesting that cellular responses to oxidative stress were partly mediated by mitochondrial dysfunction. This possibility was further validated by microarray analysis, which suggested that almost one-fourth of the cellular responses to oxidative stress were mediated by mitochondrial dysfunction that accompanies oxidative stress, thereby warranting a therapeutic strategy that targets mitochondria for the treatment of oxidative stress-associated diseases.     

Cyclin B1 mRNA translation is temporally controlled through formation and disassembly of RNA granules

Temporal control of messenger RNA (mRNA) translation is an important mechanism for regulating cellular, neuronal, and developmental processes. However, mechanisms that coordinate timing of translational activation remain largely unresolved. Full-grown oocytes arrest meiosis at prophase I and deposit dormant mRNAs. Of these, translational control of cyclin B1 mRNA in response to maturation-inducing hormone is important for normal progression of oocyte maturation, through which oocytes acquire fertility. In this study, we found that dormant cyclin B1 mRNA forms granules in the cytoplasm of zebrafish and mouse oocytes. Real-time imaging of translation revealed that the granules disassemble at the time of translational activation during maturation. Formation of cyclin B1 RNA granules requires binding of the mRNA to Pumilio1 protein and depends on actin filaments. Disruption of cyclin B1 RNA granules accelerated the timing of their translational activation after induction of maturation, whereas stabilization hindered translational activation. Thus, our results suggest that RNA granule formation is critical for the regulation of timing of translational activation.     

c-MYC-Induced Sebaceous Gland Differentiation Is Controlled by an Androgen Receptor/p53 Axis

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Highlights? Myc-induced sebaceous differentiation depends on the androgen receptor and p53 ? The androgen receptor promotes sebocyte differentiation ? Myc induces a p53 response that promotes sebocyte proliferation ? p53 and the androgen receptor are mutually antagonistic     

Regulated DNA rearrangement during sporulation in Bacillus weihenstephanensis KBAB4

Temperate phages can integrate their genomes into a specific region of a host chromosome to produce lysogens (prophage). During genome insertion, prophages may interrupt the gene coding sequence. In Bacillus subtilis, the sigma factor gene sigK is interrupted by a 48 kb prophage‐like element. sigK is a composite coding sequence from two partial genes during sporulation. For over two decades, however, no further examples of DNA element‐mediated gene reconstitution other than sigK have been identified in spore formers. Here we report that the gene for dipicolinic acid (DPA) synthetase β subunit spoVFB in B. weihenstephanensis KBAB4 is interrupted by a prophage‐like element named vfbin. DPA is synthesized in the mother cell and required for maintaining spore dormancy. We found that spoVFB was a composite coding sequence generated in the mother cell via chromosomal rearrangement that excised vfbin. Furthermore, vfbin caused excision after phage‐inducer treatment, but vfbin appeared to be defective as a prophage. We also found various spore‐forming bacteria in which sporulation‐related genes were disrupted by prophage‐like DNA elements. These results demonstrate the first example of a similar mechanism that affects a sporulation gene other than sigK and suggest that this prophage‐mediated DNA rearrangement is a common phenomenon in spore‐forming bacteria.     

Application of Fluolid-Orange-labeled probes for DNA microarray and immunological assays

The usefulness of Fluolid-Orange, a novel fluorescent dye, for DNA microarray and immunological assays has been examined. Fluolid-Orange-labeled probes (DNA and IgG) were stable as examined by laser-photo-bleaching and under heat and dry conditions. Statistical analyses were performed to evaluate the reproducibility of the microarray assay, while stage-specific immunostaining of marker proteins, Kank1 and calretinin, was performed for renal cancers, both giving satisfactory results. The stability of the dye should provide advantages for storing fluorescently labeled probes and re-examining the specimens later in genetic and pathological diagnostics.     

Semisynthesis of triptolide analogues: effect of γ-lactone and C-14 substituents on cytotoxic activities

Triptolide γ-lactone and C-14 analogues were prepared and evaluated cytotoxity against human lung adenocarcinoma epithelial A549 cells and human colon adenocarcinoma HT-29 cells. γ-Lactone substructure and C-14 substituents affected the biological activities significantly.     

N-cadherin regulates p38 MAPK signaling via association with JNK-associated leucine zipper protein: implications for neurodegeneration in Alzheimer disease

Synaptic loss, which strongly correlates with the decline of cognitive function, is one of the pathological hallmarks of Alzheimer disease. N-cadherin is a cell adhesion molecule essential for synaptic contact and is involved in the intracellular signaling pathway at the synapse. Here we report that the functional disruption of N-cadherin-mediated cell contact activated p38 MAPK in murine primary neurons, followed by neuronal death. We further observed that treatment with Aβ(42) decreased cellular N-cadherin expression through NMDA receptors accompanied by increased phosphorylation of both p38 MAPK and Tau in murine primary neurons. Moreover, expression levels of phosphorylated p38 MAPK were negatively correlated with that of N-cadherin in human brains. Proteomic analysis of human brains identified a novel interaction between N-cadherin and JNK-associated leucine zipper protein (JLP), a scaffolding protein involved in the p38 MAPK signaling pathway. We demonstrated that N-cadherin expression had an inhibitory effect on JLP-mediated p38 MAPK signal activation by decreasing the interaction between JLP and p38 MAPK in COS7 cells. Also, this study demonstrated a novel physical and functional association between N-cadherin and p38 MAPK and suggested neuroprotective roles of cadherin-based synaptic contact. The dissociation of N-cadherin-mediated synaptic contact by Aβ may underlie the pathological basis of neurodegeneration such as neuronal death, synaptic loss, and Tau phosphorylation in Alzheimer disease brain.