The role of parental achievement goals in predicting autonomy-supportive and controlling parenting

Although autonomy-supportive and controlling parenting are linked to numerous positive and negative child outcomes respectively, fewer studies have focused on their determinants. Drawing on achievement goal theory and self-determination theory, we propose that parental achievement goals (i.e., achievement goals that parents have for their children) can be mastery, performance-approach or performance-avoidance oriented and that types of goals predict mothers' tendency to adopt autonomy-supportive and controlling behaviors. A total of 67 mothers (aged 30-53 years) reported their goals for their adolescent (aged 13-16 years; 19.4 % girls), while their adolescent evaluated their mothers' behaviors. Hierarchical regression analyses showed that parental performance-approach goals predict more controlling parenting and prevent acknowledgement of feelings, one autonomy-supportive behavior. In addition, mothers who have mastery goals and who endorse performance-avoidance goals are less likely to use guilt-inducing criticisms. These findings were observed while controlling for the effect of maternal anxiety

Concordant colon tumors in monozygotic twins previously treated for prostate cancer

This report describes the quasi-simultaneous occurrence of colon cancers in monozygotic twin brothers (age 63 years) who had undergone androgen deprivation therapy for prostate cancers 4 years earlier. Concordance among male twins for both of these cancers has never been reported. Although the family history suggested possible genetic predispositions to both cancers, the twins have no evidence of the genetic alterations associated with hereditary colorectal tumors. We explore the possibility that colorectal tumorigenesis in these twins was fuelled by a combination of genetic and iatrogenic factors, in particular the androgen deprivation therapy used to treat their prostate cancers

Pan-cancer analysis of whole genomes

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale(1-3). Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter(4); identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation(5,6); analyses timings and patterns of tumour evolution(7); describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity(8,9); and evaluates a range of more-specialized features of cancer genomes(8,10-18).Peer reviewe

The emergence of sedentary behaviour physiology and its effects on the cardiometabolic profile in young and older adults

It has recently emerged that sedentary behaviour is independent of a lack of physical activity as individuals can be sufficiently active, based on the recommended physical activity guidelines, but also spend the majority of their waking hours engaging in sedentary behaviour. Individuals who follow this pattern of physical activity and sedentary behaviour are known as ‘active couch potatoes’. Sedentary behaviour has been found to have detrimental effects on cardiometabolic markers associated with cardiovascular disease. Since the positive effects of moderate-to-vigorous intensity physical activity do not necessarily negate the deleterious effects of sedentary behaviour on cardiometabolic markers, it is postulated that engaging in light physical activity is an intervention that will successfully reduce levels of sedentary behaviour and may hence improve health markers of quality of life. We propose that such lifestyle changes may be particularly relevant to older populations as these engage in sedentary behaviour for the majority of their waking hours, thereby adding to the negative aging effect on cardiometabolic markers

Epidemiology of perforated colonic diverticular disease

Perforated colonic diverticular disease results in considerable mortality and morbidity. This review appraises existing evidence on the epidemiology and mechanisms of perforation, highlights areas of further study, and suggests an epidemiological approach towards preventing the condition. Computerised searches were used to identify published articles relating to the epidemiology, pathophysiology, and clinical features of perforated colonic diverticular disease. Several drug and dietary exposures have potential biological mechanisms for causing perforation. Of these only non-steroidal anti-inflammatory drugs have been consistently identified as risk factors in aetiological studies. The causes of perforated colonic diverticular disease remain largely unknown. Further aetiological studies, looking specifically at perforation, are required to investigate whether cause-effect relationships exist for both drug and dietary exposures. The identification of risk factors for perforation would allow primary public health prevention, secondary risk factor modification, and early prophylactic surgery to be aimed at people at high risk