The association between divorce and patterns of child adjustment

Previous research has indicated that although children from divorced families on average are not as well adjusted as children from intact families, there is a great deal of variability in how these children adjust to the divorce of their parents. In an effort to investigate the within-group variability of children of divorced families the generalizability of clusters of adjustment found by E. M. Hetherington (1989, 1993) was investigated. Data were gathered from 137 boys and girls primarily between the ages of 12-14 years. Participants came from both divorced and intact families. Measures included the Child Behavior Checklist - Youth Self-Report (YSR), the Bar-On Emotional Quotient Inventory: Youth Version (EQ-I: YV), a measure of students' sense of school values and competence (SSVC), and an interview focusing on parents' marital histories. Data for the main sample were submitted to a squared Euclidean cluster analysis using Ward's method of agglomeration. The stability and validity of the derived clusters was investigated via internal replication and a double-cross validation using multiple discriminant analysis. The clusters obtained from the main sample did not evidence a high level of consistency across different subsets of the sample and the correct classification rates were low thus indicating a lack of homogeneity within clusters and discreteness between clusters. No evidence was found for distinct patterns of adjustment within the sample. Possible explanations for the findings are discussed along with the issue of obtaining an adequate sample of children from divorced families

Structured leisure and adolescent adjustment

The relationships between participation in structured leisure (SL) activities (e.g., sports, prosocial activities) and adolescent adjustment were investigated. SL activities have been associated with various developmental benefits but there has been a limited number of studies that have investigated the potential negative aspects of participation. Questionnaire data were collected from 210 boys and girls (between grades 10 and 12). Fourteen students participated in focus groups to obtain a phenomenological perspective on SL participation. Adjustment variables included a well-being composite (comprised of depression, anxiety, self-esteem, and life satisfaction), a school orientation composite (comprised of students’ levels of school involvement and their values regarding school), academic achievement, and self-oriented and socially prescribed perfectionism. Three hypotheses were examined. First, it was predicted that there would be a curvilinear relationship between the extent of SL participation and the various adjustment variables. Second, aspects of play and leisure were expected to have moderating effects on the relationships between SL participation and outcomes. Third, aspects of perfectionism were hypothesized to play a moderating role on the relationship between SL and adolescent adjustment. Although the present investigation yielded some insightful observations about participation in SL activities, the results provided no direct support for the hypotheses. Regression analyses indicated positive relationships between SL participation and self-oriented perfectionism, and SL participation and academic achievement. Negative relationships were found between the degree of playfulness in SL activities and socially prescribed perfectionism, and between academic achievement and global intrinsic leisure motivation. Notable focus group themes included a distinction between the fun experienced in SL activities and the fun experienced in nonstructured contexts, significant positive and negative experiences related to SL participation, and differences and similarities between the SL context and other contexts such as school. It is argued that leisure theory can contribute to a better understanding of the developmental implications of SL participation and that the relationship between SL participation and perfectionism merits further investigation

Public Sector Governance in Australia

Australia lacks a scholarly book that covers recent developments in public sector governance in Australia and blends cross-disciplinary perspectives from law, management, public administration and public policy. The primary reason for writing this book is to fill the gap in the treatment of this subject, and to provide insights from empirical evidence and current practice. The book provides the first comprehensive theoretical and empirical work on governance in the Commonwealth public sector. It addresses the issues that emerged under the Howard government as well as their handling under the Rudd and Gillard governments. The book aims to enhance understanding of and communication about public governance across government, industry and the community. The authors bring to this book expertise gained from political science, public administration and policy, public and private sector law

Sustained expression of microRNA-155 in hematopoietic stem cells causes a myeloproliferative disorder

Mammalian microRNAs are emerging as key regulators of the development and function of the immune system. Here, we report a strong but transient induction of miR-155 in mouse bone marrow after injection of bacterial lipopolysaccharide (LPS) correlated with granulocyte/monocyte (GM) expansion. Demonstrating the sufficiency of miR-155 to drive GM expansion, enforced expression in mouse bone marrow cells caused GM proliferation in a manner reminiscent of LPS treatment. However, the miR-155–induced GM populations displayed pathological features characteristic of myeloid neoplasia. Of possible relevance to human disease, miR-155 was found to be overexpressed in the bone marrow of patients with certain subtypes of acute myeloid leukemia (AML). Furthermore, miR-155 repressed a subset of genes implicated in hematopoietic development and disease. These data implicate miR-155 as a contributor to physiological GM expansion during inflammation and to certain pathological features associated with AML, emphasizing the importance of proper miR-155 regulation in developing myeloid cells during times of inflammatory stress

Cell autonomous regulation of herpes and influenza virus infection by the circadian clock.

Viruses are intracellular pathogens that hijack host cell machinery and resources to replicate. Rather than being constant, host physiology is rhythmic, undergoing circadian (∼24 h) oscillations in many virus-relevant pathways, but whether daily rhythms impact on viral replication is unknown. We find that the time of day of host infection regulates virus progression in live mice and individual cells. Furthermore, we demonstrate that herpes and influenza A virus infections are enhanced when host circadian rhythms are abolished by disrupting the key clock gene transcription factor Bmal1. Intracellular trafficking, biosynthetic processes, protein synthesis, and chromatin assembly all contribute to circadian regulation of virus infection. Moreover, herpesviruses differentially target components of the molecular circadian clockwork. Our work demonstrates that viruses exploit the clockwork for their own gain and that the clock represents a novel target for modulating viral replication that extends beyond any single family of these ubiquitous pathogens.A.B.R. acknowledges funding from the Wellcome Trust (083643/Z/07/Z, 100333/Z/12/Z and 100574/Z/12/Z), the European Research Council (ERC Starting Grant No. 281348, MetaCLOCK), the EMBO Young Investigators Programme, the Lister Institute of Preventative Medicine and the Medical Research Council (MRC_MC_UU_12012/5). A.D.N acknowledges funding from the People Programme (Marie Curie Actions) of the European Union Seventh Framework Programme (FP7/2007-2013; REA grant agreement 627630). We thank L. Ansel-Bollepalli for assistance with animal breeding, I. Robinson for assistance with pilot animal experiments, A. Snijders and H. Flynn (Francis Crick Institute Proteomics Core) for help with proteomics work, Cambridge NIHR BRC Cell Phenotyping Hub for flow cytometry assistance, A. Miyawaki (RIKEN Brain Science Institute, Japan) for Fucci2 lentiviral vectors, and H. Coleman, J. May and M. Jain for helpful discussions. We thank Prof J. Bass (Northwestern University, USA) for Bmal-/- mouse embryonic fibroblasts used in preliminary experiments, and N. Heaton and P. Palese (Icahn School of Medicine at Mount Sinai, USA) for PB2::Gaussia luciferase IAV (PR8 PB2::GLUC).This is the author accepted manuscript. The final version is available from the National Academy of Sciences via http://dx.doi.org/10.1073/pnas.160189511

Cellular Models of Aggregation-Dependent Template-Directed Proteolysis to Characterize Tau Aggregation Inhibitors for Treatment of Alzheimer's Disease

Copyright © 2015, The American Society for Biochemistry and Molecular Biology. Acknowledgements-We thank Drs Timo Rager and Rolf Hilfiker (Solvias, Switzerland) for polymorph analyses.Peer reviewedPublisher PD

Clinical practice guidelines on hemochromatosis: Asian Pacific Association for the Study of the Liver

Hereditary hemochromatosis is the result of pathogenic variants in multiple genes that can result in increased body iron stores with excess iron deposited in various organs, including the liver, pancreas, and heart. The two most important advances in the field over the past 30 years have been the identification of the HFE gene (and the associated p.Cys282Tyr substitution), and the discovery of the hormone hepcidin, which is inappropriately low in this condition and is the pathophysiological basis of the increased iron absorption. The identification of mutations in the HFE gene and subsequent studies have reshaped diagnostic algorithms resulting in a marked reduction in the need for liver biopsy. The discovery of hepcidin has resulted in many studies that have dramatically improved our understanding of iron metabolism with clear potential therapeutic implications. The variable clinical expression of hemochromatosis has puzzled clinicians and scientists, and our understanding of the factors that influence the phenotype has increased over recent years. Nevertheless, increased clinician and patient awareness, early diagnosis, and therapeutic phlebotomy to restore normal life expectancy are still the cornerstones of management. The classic triad of cirrhosis, diabetes, and skin pigmentation is now uncommon, and many patients are diagnosed with minimal or no symptoms

The heme-hemopexin scavenging system is active in the brain, and associates with outcome after subarachnoid hemorrhage

Background and Purpose – Long-term outcome after subarachnoid hemorrhage (SAH) is potentially linked to cytotoxic heme. Free heme is bound by hemopexin (Hpx) and rapidly scavenged by CD91. We hypothesized that heme scavenging in the brain would be associated with outcome after haemorrhage. Methods - Using cerebrospinal fluid (CSF) and tissue from SAH patients and control individuals, the activity of the intracranial CD91-Hpx system was examined using enzyme-linked immunoassays, ultra-high performance liquid chromatography and immunohistochemistry. Results - In control individuals, CSF Hpx was mainly synthesized intrathecally. After SAH, CSF Hpx was high in one-third of cases, and these patients had a higher probability of delayed cerebral ischaemia and poorer neurological outcome. The intracranial CD91-Hpx system was active after SAH since CD91 positively correlated with iron deposition in brain tissue. Heme-Hpx uptake saturated rapidly after SAH, since bound heme accumulated early in the CSF. When the blood-brain barrier was compromised following SAH, serum Hpx level was lower, suggesting heme transfer to the circulation for peripheral CD91 scavenging. Conclusions - The CD91-heme-Hpx scavenging system is important after SAH and merits further study as a potential prognostic marker and therapeutic target