Posttraumatic Growth As It Relates To Family Environment

The current study sought to explore the relationship between one\u27s family environment and reported posttraumatic growth. Participants were 197 EKU undergraduate intro to psychology students. They voluntarily took an online survey for course credit. Types and frequency of trauma was recorded using the Life Events Checklist. The Posttraumatic Growth Index was used to measure posttraumatic growth, the Family environment scale was used to assess qualities of family life, and the Big Five Inventory was used to control for personality traits. Results did not support the hypothesis, however, significant correlations with the Moral Religious subscale of the FES as well as neuroticism and openness factors of the BFI were found. Implications of these results are discussed

Finding Confidence, Balance, and Self-acceptance: a Clinician’s Guide to Treating Involuntary Celibates

Involuntary Celibates (incels) are a new and poorly understood population. In the field of psychology, very little research has been done on the population, and even fewer clinicians have successfully worked with clients from this group. This handbook was created in an attempt to outline the history, belief system, terminology, and common mental health problems of incels and their related groups. This information is distilled down and presented as a primer for anyone looking to understand this new population. Also, possible treatment recommendations are suggested and discussed in detail based on the particular psychological difficulties that incels often face

Evidence for the unique pathological classification of mutant S0D1-ALS

Amyotrophic lateral sclerosis [ALS] is a neurological disease characterized by the selective loss of motor neurons [MNs] and death due to respiratory failure usually occurs within 3-5 years of symptom onset. Mutations in the genes encoding TAR DNA binding protein of 43 kDa [TDP-43], fused in sarcoma/translocated in liposarcoma [FUS/TLS] and Cu/Zn superoxide dismutase [SOD1] have all been associated with ALS. Never before has a link been made between the variant of ALS and intraneuronal pathology. This thesis has sought to (1) analyze the immunohistochemical expression of TDP-43, FUS/TLS, SOD1, Rho Guanine nucleotide exchange factor [RGNEF], and 5 other ALS-associated proteins across multiple variants of ALS, and (2) characterize the immunohistochemical expression of RGNEF for the first time. Here, I show that mutant SOD1-ALS is a pathologically unique variant of ALS. This finding may be used in the identification of novel families that may be at risk for developing ALS

Approximating invariant densities of metastable systems

We consider a piecewise smooth expanding map of the interval possessing two invariant subsets of positive Lebesgue measure and exactly two ergodic absolutely continuous invariant probability measures (ACIMs). When this system is perturbed slightly to make the invariant sets merge, we describe how the unique ACIM of the perturbed map can be approximated by a convex combination of the two initial ergodic ACIMs.Comment: 19 pages, 6 figure

Causal graphical models in systems genetics: A unified framework for joint inference of causal network and genetic architecture for correlated phenotypes

Causal inference approaches in systems genetics exploit quantitative trait loci (QTL) genotypes to infer causal relationships among phenotypes. The genetic architecture of each phenotype may be complex, and poorly estimated genetic architectures may compromise the inference of causal relationships among phenotypes. Existing methods assume QTLs are known or inferred without regard to the phenotype network structure. In this paper we develop a QTL-driven phenotype network method (QTLnet) to jointly infer a causal phenotype network and associated genetic architecture for sets of correlated phenotypes. Randomization of alleles during meiosis and the unidirectional influence of genotype on phenotype allow the inference of QTLs causal to phenotypes. Causal relationships among phenotypes can be inferred using these QTL nodes, enabling us to distinguish among phenotype networks that would otherwise be distribution equivalent. We jointly model phenotypes and QTLs using homogeneous conditional Gaussian regression models, and we derive a graphical criterion for distribution equivalence. We validate the QTLnet approach in a simulation study. Finally, we illustrate with simulated data and a real example how QTLnet can be used to infer both direct and indirect effects of QTLs and phenotypes that co-map to a genomic region.Comment: Published in at http://dx.doi.org/10.1214/09-AOAS288 the Annals of Applied Statistics (http://www.imstat.org/aoas/) by the Institute of Mathematical Statistics (http://www.imstat.org