Factors associated with the successful removal of indwelling urinary catheters post-operatively in the fragility hip fracture patient

Introduction Patients presenting to hospital with a fragility hip fracture are routinely catheterized in the emergency department. Studies have found that the duration of catheterization is the greatest and most important risk factor for developing a urinary tract infection. Whilst there is a considerable body of evidence around correct techniques for insertion of urinary catheters, there appears to be little evidence as to the timing of their removal. Aim of the study To describe the current practice of indwelling catheter (IDC) removal post operatively in the fragility hip fracture patient and to identify factors associated with the successful removal of IDCs post operatively in the same cohort of patients. Methods This study was a retrospective cohort analysis of patients admitted to a large, tertiary hospital with an established ortho-geriatric model of care. Results Aperient regime was the only factor that appeared to have a significant impact on the successful IDC removal. The patient commenced on the aperient regime was three times more likely to have an unsuccessful IDC removal than the patient on a limited or no aperient regime. Conclusion This study highlights the need for redesigning care that is patient focused, evidence-based, effective and efficient. The argument that a patient's bowel is required to be emptied prior to the successful removal of an IDC appears to be false, as in this study it was not identified as a predictor of successful IDC removal. A prospective clinical trial may be the next step forward in developing a clinical guideline for the successful removal of IDCs in the fragility hip fracture patient and/or surgical patient. Nurses have a crucial role to play in contributing to evidence-based practice and are continually challenged to do so

Genome-wide association study identifies 30 loci associated with bipolar disorder.

Bipolar disorder is a highly heritable psychiatric disorder. We performed a genome-wide association study (GWAS) including 20,352 cases and 31,358 controls of European descent, with follow-up analysis of 822 variants with P < 1 × 10-4 in an additional 9,412 cases and 137,760 controls. Eight of the 19 variants that were genome-wide significant (P < 5 × 10-8) in the discovery GWAS were not genome-wide significant in the combined analysis, consistent with small effect sizes and limited power but also with genetic heterogeneity. In the combined analysis, 30 loci were genome-wide significant, including 20 newly identified loci. The significant loci contain genes encoding ion channels, neurotransmitter transporters and synaptic components. Pathway analysis revealed nine significantly enriched gene sets, including regulation of insulin secretion and endocannabinoid signaling. Bipolar I disorder is strongly genetically correlated with schizophrenia, driven by psychosis, whereas bipolar II disorder is more strongly correlated with major depressive disorder. These findings address key clinical questions and provide potential biological mechanisms for bipolar disorder

Genomic Relationships, Novel Loci, and Pleiotropic Mechanisms across Eight Psychiatric Disorders

Genetic influences on psychiatric disorders transcend diagnostic boundaries, suggesting substantial pleiotropy of contributing loci. However, the nature and mechanisms of these pleiotropic effects remain unclear. We performed analyses of 232,964 cases and 494,162 controls from genome-wide studies of anorexia nervosa, attention-deficit/hyper-activity disorder, autism spectrum disorder, bipolar disorder, major depression, obsessive-compulsive disorder, schizophrenia, and Tourette syndrome. Genetic correlation analyses revealed a meaningful structure within the eight disorders, identifying three groups of inter-related disorders. Meta-analysis across these eight disorders detected 109 loci associated with at least two psychiatric disorders, including 23 loci with pleiotropic effects on four or more disorders and 11 loci with antagonistic effects on multiple disorders. The pleiotropic loci are located within genes that show heightened expression in the brain throughout the lifespan, beginning prenatally in the second trimester, and play prominent roles in neurodevelopmental processes. These findings have important implications for psychiatric nosology, drug development, and risk prediction.Peer reviewe

The genetics of the mood disorder spectrum:genome-wide association analyses of over 185,000 cases and 439,000 controls

Background Mood disorders (including major depressive disorder and bipolar disorder) affect 10-20% of the population. They range from brief, mild episodes to severe, incapacitating conditions that markedly impact lives. Despite their diagnostic distinction, multiple approaches have shown considerable sharing of risk factors across the mood disorders. Methods To clarify their shared molecular genetic basis, and to highlight disorder-specific associations, we meta-analysed data from the latest Psychiatric Genomics Consortium (PGC) genome-wide association studies of major depression (including data from 23andMe) and bipolar disorder, and an additional major depressive disorder cohort from UK Biobank (total: 185,285 cases, 439,741 controls; non-overlapping N = 609,424). Results Seventy-three loci reached genome-wide significance in the meta-analysis, including 15 that are novel for mood disorders. More genome-wide significant loci from the PGC analysis of major depression than bipolar disorder reached genome-wide significance. Genetic correlations revealed that type 2 bipolar disorder correlates strongly with recurrent and single episode major depressive disorder. Systems biology analyses highlight both similarities and differences between the mood disorders, particularly in the mouse brain cell-types implicated by the expression patterns of associated genes. The mood disorders also differ in their genetic correlation with educational attainment – positive in bipolar disorder but negative in major depressive disorder. Conclusions The mood disorders share several genetic associations, and can be combined effectively to increase variant discovery. However, we demonstrate several differences between these disorders. Analysing subtypes of major depressive disorder and bipolar disorder provides evidence for a genetic mood disorders spectrum

Bipolar multiplex families have an increased burden of common risk variants for psychiatric disorders.

Multiplex families with a high prevalence of a psychiatric disorder are often examined to identify rare genetic variants with large effect sizes. In the present study, we analysed whether the risk for bipolar disorder (BD) in BD multiplex families is influenced by common genetic variants. Furthermore, we investigated whether this risk is conferred mainly by BD-specific risk variants or by variants also associated with the susceptibility to schizophrenia or major depression. In total, 395 individuals from 33 Andalusian BD multiplex families (166 BD, 78 major depressive disorder, 151 unaffected) as well as 438 subjects from an independent, BD case/control cohort (161 unrelated BD, 277 unrelated controls) were analysed. Polygenic risk scores (PRS) for BD, schizophrenia (SCZ), and major depression were calculated and compared between the cohorts. Both the familial BD cases and unaffected family members had higher PRS for all three psychiatric disorders than the independent controls, with BD and SCZ being significant after correction for multiple testing, suggesting a high baseline risk for several psychiatric disorders in the families. Moreover, familial BD cases showed significantly higher BD PRS than unaffected family members and unrelated BD cases. A plausible hypothesis is that, in multiplex families with a general increase in risk for psychiatric disease, BD development is attributable to a high burden of common variants that confer a specific risk for BD. The present analyses demonstrated that common genetic risk variants for psychiatric disorders are likely to contribute to the high incidence of affective psychiatric disorders in the multiplex families. However, the PRS explained only part of the observed phenotypic variance, and rare variants might have also contributed to disease development

Genetic Overlap Between Alzheimer’s Disease and Bipolar Disorder Implicates the MARK2 and VAC14 Genes

Background: Alzheimer's disease (AD) and bipolar disorder (BIP) are complex traits influenced by numerous common genetic variants, most of which remain to be detected. Clinical and epidemiological evidence suggest that AD and BIP are related. However, it is not established if this relation is of genetic origin. Here, we applied statistical methods based on the conditional false discovery rate (FDR) framework to detect genetic overlap between AD and BIP and utilized this overlap to increase the power to identify common genetic variants associated with either or both traits. Methods: We obtained genome wide association studies data from the International Genomics of Alzheimer's Project part 1 (17,008 AD cases and 37,154 controls) and the Psychiatric Genetic Consortium Bipolar Disorder Working Group (20,352 BIP cases and 31,358 controls). We used conditional QQ-plots to assess overlap in common genetic variants between AD and BIP. We exploited the genetic overlap to re-rank test-statistics for AD and BIP and improve detection of genetic variants using the conditional FDR framework. Results: Conditional QQ-plots demonstrated a polygenic overlap between AD and BIP. Using conditional FDR, we identified one novel genomic locus associated with AD, and nine novel loci associated with BIP. Further, we identified two novel loci jointly associated with AD and BIP implicating the MARK2 gene (lead SNP rs10792421, conjunctional FDR=0.030, same direction of effect) and the VAC14 gene (lead SNP rs11649476, conjunctional FDR=0.022, opposite direction of effect). Conclusions: We found polygenic overlap between AD and BIP and identified novel loci for each trait and two jointly associated loci. Further studies should examine if the shared loci implicating the MARK2 and VAC14 genes could explain parts of the shared and distinct features of AD and BIP

Genomic Dissection of Bipolar Disorder and Schizophrenia, Including 28 Subphenotypes

publisher: Elsevier articletitle: Genomic Dissection of Bipolar Disorder and Schizophrenia, Including 28 Subphenotypes journaltitle: Cell articlelink: https://doi.org/10.1016/j.cell.2018.05.046 content_type: article copyright: © 2018 Elsevier Inc

Taxonomic and Nomenclatural Changes in the Pelidnotine Scarabs (Coleoptera: Scarabaeidae: Rutelinae: Rutelini)

Click on the DOI link to access the article (may not be free).The taxonomy and nomenclature of several species-group names for the pelidnotine scarabs (Scarabaeidae: Rutelinae: Rutelini) are clarified. Two replacement names are proposed for homonyms in the genus Pelidnota MacLeay: Pelidnota francoisgenieri Moore and Jameson, new name, for Pelidnota genieri Soula, 2009 and Pelidnota vladimalyi Moore and Jameson, new name, for Pelidonota malyi Soula, 2010. Two replacement names are proposed for homonyms in the genus Patatra Soula: Neopatatra Moore and Jameson, new name and new synonym, for Patatra Soula, 2009 and Patatra synonyma Moore and Jameson, new name and new synonym, for Patatra mathani Soula, 2009. The genus Minilasiocala Soula is a new synonym of Microogenius Gutierrez. The nomenclature of the genus Hoplopelidnota F. Bates is clarified, and Hoplopelidnota armata Ohaus is a new synonym of Hoplopelidnota metallica Laporte. The genus Pelidnotopsis Ohaus is considered a new synonym of Chrysina Kirby. The following names are unavailable: Epichalcoplethis vazdemelli Soula, Mecopelidnota willersi Soula, Pelidnota demergesi Soula, Pelidnota vladislavmalyi Soula, and Sorocha damasoi satipoensis Soula. Chrysina henrybatesi Hawks, 2001 is considered a nomen nudum and an unavailable name. Two names are emended: the spelling of Plusiotis turckheimi Ohaus is emended to Chrysina tuerckheimi and Chalcoplethis kirbyi misionesensis Soula (an incorrect original spelling) is emended to Chalcoplethis kirbii misionesensis. The status of infrasubspecific names in the pelidnotine scarabs is discussed. The name Pelidnota semiaurata var. citripennis (Ohaus) is elevated to Pelidnota semiaurata citripennis (Ohaus), new status. Parhoplognathus parvulus var. rubripennis Ohaus is infrasubspecific and an unavailable name. The name Parhoplognathus rubripennis should be attributed to Soula and not Ohaus. The three varieties of Pelidnota cuprea described by Ohaus are infrasubspecific and are unavailable names. A list of subsequent incorrect spellings in the pelidnotine scarabs, a list of lapsus calami from Soula's four volumes on the pelidnotines, and a list of genera included in the pelidnotine scarabs sensu Soula are provided