PLCG2 variants in cherubism.

BACKGROUND: Cherubism is most commonly caused by rare heterozygous gain-of-function (GOF) missense variants in SH3BP2, which appear to signal through phospholipase C gamma 2 (PLCG2) to cause excessive osteoclast activity leading to expansile lesions in facial bones in childhood. GOF variants in PLCG2 lead to autoinflammatory PLCG2-associated antibody deficiency and immune dysregulation (autoinflammatory PLAID, or PLAID-GOF), characterized by variably penetrant autoinflammatory, autoimmune, infectious, and atopic manifestations. Cherubism has not been reported in PLAID to date. OBJECTIVE: We determined whether GOF PLCG2 variants may be associated with cherubism. METHODS: Clinical, laboratory, and genomic data from 2 patients with cherubism and other clinical symptoms observed in patients with PLCG2 variants were reviewed. Primary B-cell receptor-induced calcium flux was assessed by flow cytometry. RESULTS: Two patients with lesions consistent with cherubism but no SH3BP2 variants were found to have rare PLCG2 variants previously shown to be GOF in vitro, leading to increased primary B-cell receptor-induced calcium flux in one patient's B cells. Variable humoral defects, autoinflammatory rash, and other clinical and laboratory findings consistent with PLAID were observed as well. CONCLUSION: GOF PLCG2 variants likely represent a novel genetic driver of cherubism and should be assessed in SH3BP2-negative cases. Expansile bony lesions expand the phenotypic landscape of autoinflammatory PLAID, and bone imaging should be considered in PLAID patients.

Relationship between polygenic risk scores and symptom dimensions of schizophrenia and schizotypy in multiplex families with schizophrenia.

BACKGROUND: Psychotic disorders and schizotypal traits aggregate in the relatives of probands with schizophrenia. It is currently unclear how variability in symptom dimensions in schizophrenia probands and their relatives is associated with polygenic liability to psychiatric disorders. AIMS: To investigate whether polygenic risk scores (PRSs) can predict symptom dimensions in members of multiplex families with schizophrenia. METHOD: The largest genome-wide data-sets for schizophrenia, bipolar disorder and major depressive disorder were used to construct PRSs in 861 participants from the Irish Study of High-Density Multiplex Schizophrenia Families. Symptom dimensions were derived using the Operational Criteria Checklist for Psychotic Disorders in participants with a history of a psychotic episode, and the Structured Interview for Schizotypy in participants without a history of a psychotic episode. Mixed-effects linear regression models were used to assess the relationship between PRS and symptom dimensions across the psychosis spectrum. RESULTS: Schizophrenia PRS is significantly associated with the negative/disorganised symptom dimension in participants with a history of a psychotic episode (P = 2.31 × 10-4) and negative dimension in participants without a history of a psychotic episode (P = 1.42 × 10-3). Bipolar disorder PRS is significantly associated with the manic symptom dimension in participants with a history of a psychotic episode (P = 3.70 × 10-4). No association with major depressive disorder PRS was observed. CONCLUSIONS: Polygenic liability to schizophrenia is associated with higher negative/disorganised symptoms in participants with a history of a psychotic episode and negative symptoms in participants without a history of a psychotic episode in multiplex families with schizophrenia. These results provide genetic evidence in support of the spectrum model of schizophrenia, and support the view that negative and disorganised symptoms may have greater genetic basis than positive symptoms, making them better indices of familial liability to schizophrenia.

Differences in genetic correlations between posttraumatic stress disorder and alcohol-related problems phenotypes compared to alcohol consumption-related phenotypes.

BACKGROUND: Posttraumatic Stress Disorder (PTSD) tends to co-occur with greater alcohol consumption as well as alcohol use disorder (AUD). However, it is unknown whether the same etiologic factors that underlie PTSD-alcohol-related problems comorbidity also contribute to PTSD- alcohol consumption. METHODS: We used summary statistics from large-scale genome-wide association studies (GWAS) of European-ancestry (EA) and African-ancestry (AA) participants to estimate genetic correlations between PTSD and a range of alcohol consumption-related and alcohol-related problems phenotypes. RESULTS: In EAs, there were positive genetic correlations between PTSD phenotypes and alcohol-related problems phenotypes (e.g. Alcohol Use Disorders Identification Test (AUDIT) problem score) (rGs: 0.132-0.533, all FDR adjusted p < 0.05). However, the genetic correlations between PTSD phenotypes and alcohol consumption -related phenotypes (e.g. drinks per week) were negatively associated or non-significant (rGs: -0.417 to -0.042, FDR adjusted p: <0.05-NS). For AAs, the direction of correlations was sometimes consistent and sometimes inconsistent with that in EAs, and the ranges were larger (rGs for alcohol-related problems: -0.275 to 0.266, FDR adjusted p: NS, alcohol consumption-related: 0.145-0.699, FDR adjusted p: NS). CONCLUSIONS: These findings illustrate that the genetic associations between consumption and problem alcohol phenotypes and PTSD differ in both strength and direction. Thus, the genetic factors that may lead someone to develop PTSD and high levels of alcohol consumption are not the same as those that lead someone to develop PTSD and alcohol-related problems. Discussion around needing improved methods to better estimate heritabilities and genetic correlations in diverse and admixed ancestry samples is provided.

Associations Between Traumatic Stress, Brain Volumes and Post-traumatic Stress Disorder Symptoms in Children: Data from the ABCD Study.

Reduced volumes in brain regions of interest (ROIs), primarily from adult samples, are associated with posttraumatic stress disorder (PTSD). We extended this work to children using data from the Adolescent Brain Cognitive Development (ABCD) Study® (N = 11,848; Mage = 9.92). Structural equation modeling and an elastic-net (EN) machine-learning approach were used to identify potential effects of traumatic events (TEs) on PTSD symptoms (PTSDsx) directly, and indirectly via the volumes 300 subcortical and cortical ROIs. We then estimated the genetic and environmental variation in the phenotypes. TEs were directly associated with PTSDsx (r = 0.92) in children, but their indirect effects (r < 0.0004)-via the volumes of EN-identified subcortical and cortical ROIs-were negligible at this age. Additive genetic factors explained a modest proportion of the variance in TEs (23.4%) and PTSDsx (21.3%), and accounted for most of the variance of EN-identified volumes of four of the five subcortical (52.4-61.8%) three of the nine cortical ROIs (46.4-53.3%) and cerebral white matter in the left hemisphere (57.4%). Environmental factors explained most of the variance in TEs (C = 61.6%, E = 15.1%), PTSDsx (residual-C = 18.4%, residual-E = 21.8%), right lateral ventricle (C = 15.2%, E = 43.1%) and six of the nine EN-identified cortical ROIs (C = 4.0-13.6%, E = 56.7-74.8%). There is negligible evidence that the volumes of brain ROIs are associated with the indirect effects of TEs on PTSDsx at this age. Overall, environmental factors accounted for more of the variation in TEs and PTSDsx. Whereas additive genetic factors accounted for most of the variability in the volumes of a minority of cortical and in most of subcortical ROIs.

Wnt5a promotes differentiation and development of adult-born neurons in the hippocampus by noncanonical Wnt signaling.

In the adult hippocampus, new neurons are generated in the dentate gyrus. The Wnt signaling pathway regulates this process, but little is known about the endogenous Wnt ligands involved. We investigated the role of Wnt5a on adult hippocampal neurogenesis. Wnt5a regulates neuronal morphogenesis during embryonic development, and maintains dendritic architecture of pyramidal neurons in the adult hippocampus. Here, we determined that Wnt5a knockdown in the mouse dentate gyrus by lentivirus-mediated shRNA impaired neuronal differentiation of progenitor cells, and reduced dendritic development of adult-born neurons. In cultured adult hippocampal progenitors (AHPs), Wnt5a knockdown reduced neuronal differentiation and morphological development of AHP-derived neurons, whereas treatment with Wnt5a had the opposite effect. Interestingly, no changes in astrocytic differentiation were observed in vivo or in vitro, suggesting that Wnt5a does not affect fate-commitment. By using specific inhibitors, we determined that Wnt5a signals through CaMKII to induce neurogenesis, and promotes dendritic development of newborn neurons through activating Wnt/JNK and Wnt/CaMKII signaling. Our results indicate Wnt5a as a niche factor in the adult hippocampus that promotes neuronal differentiation and development through activation of noncanonical Wnt signaling pathways.

Psychiatric Resilience and Alcohol Resistance: A Twin Study of Genetic Correlation and Sex Differences.

Variability in psychiatric response following stressful/traumatic life events is frequently observed. There is also variability in propensity for alcohol use disorder (AUD) such that some can consume substantial amounts and not develop AUD symptoms whereas others develop an AUD. Our group has applied discrepancy-based approaches to capture psychiatric resilience (PR) and alcohol resistance (AR), both moderately heritable. This study sought to (1) examine the genetic and environmental correlation of these constructs and (2) model qualitative and quantitative sex effects. Data came from a large twin sample (N = 4501 twin pairs) with self-report measures and interviews assessing distress symptoms, stressful life events, alcohol use, and AUD. Correlated liability model results suggested a moderate degree of genetic correlation between PR and AR (0.54) due to the same genetic factors in males and females. Findings highlight the shared genetic predisposition of these resilience/resistance constructs while emphasizing the impact of unique environmental experiences.

Potential causal effect of posttraumatic stress disorder on alcohol use disorder and alcohol consumption in individuals of European descent: A Mendelian Randomization Study.

BACKGROUND: Posttraumatic stress disorder (PTSD) often co-occurs with alcohol consumption (AC) and alcohol use disorder (AUD). However, it is unknown whether the same etiologic influences that underlie PTSD co-occurring with AUD are those that underlie PTSD and AC individually. METHODS: This study used large-scale genome-wide association study (GWAS) data to test whether PTSD and drinks per week [DPW]/AUD are causally related to one another, and, if so, whether PTSD precedes DPW/AUD and/or vice versa. We used Mendelian Randomization methods to analyze European ancestry GWAS summary statistics from the Psychiatric Genomics Consortium (PGC; PTSD), GWAS & Sequencing Consortium of Alcohol and Nicotine Use (GSCAN; DPW), and the Million Veteran Program (MVP; AUD). RESULTS: PTSD exerted a potentially causal effect on AUD (ß = 0.039, SE = 0.014, p = 0.005), but not on DPW (ß = 0.002, SE = 0.003, p = 0.414). Additionally, neither DPW (ß = 0.019, SE = 0.041, p = 0.637) nor AUD (ß = 8.87 × 10-4 , SE = 0.001, p = 0.441) exerted a causal effect on PTSD. CONCLUSIONS: These findings are consistent with the self-medication model, in which individuals misuse alcohol to cope with aversive trauma-related symptoms. These findings extend latent analysis and molecular findings of shared and correlated risk between PTSD and alcohol phenotypes. Given the health behaviors associated with these phenotypes, these findings are important in that they suggest groups to prioritize for prevention efforts. Further, they provide a rationale for future preclinical and clinical studies examining the biological mechanisms by which PTSD may impact AUD.

Genetic influences on testosterone and PTSD.

Females are twice as likely to experience PTSD as compared to males. Although sex differences in prevalence are well-established, little is known about why such sex differences occur. Biological factors that vary with sex, including sex hormone production, may contribute to these differences. Considerable evidence links sex hormones, such as testosterone, to PTSD risk though less is known about the shared genetic underpinnings. The objective of the present study was to test for genetic relationships between testosterone and PTSD. To do so, we used summary statistics from large, publicly available genetic consortia to conduct linkage disequilibrium score regression to estimate the genetic correlations between PTSD and testosterone in males and females, and two-sample, bi-directional Mendelian randomization to examine potential causal relationships of testosterone on PTSD and the reverse. Heritability estimates of testosterone were significantly higher in males (0.17, SE = 0.02) than females (0.11, SE = 0.01; z = 2.46, p = 00.01). The correlation between testosterone and PTSD was negative in males (rg = -0.11, SE = 0.02, p = 6.7 x 10-6), but not significant in females (rg = 0.002, SE = 0.03, p = 0.95). MR analyses found no evidence of a causal effect of testosterone on PTSD or the reverse. Findings are consistent with phenotypic literature suggesting a relationship between testosterone and PTSD that may be sex-specific. This work provides early evidence of a relationship between testosterone and PTSD genotypically and suggests an avenue for future research that will enable a better understanding of disparities in PTSD.

The impact of the COVID-19 pandemic on alcohol use disorder symptoms: Testing interactions with polygenic risk.

Objective: The purpose of this study was to test whether COVID impact interacts with genetic risk (polygenic risk score/PRS) to predict alcohol use disorder (AUD) symptoms. Method: Participants were n = 455 college students (79.6% female, 51% European Ancestry/EA, 24% African Ancestry/AFR, 25% Americas Ancestry/AMER) from a longitudinal study during the initial stage (March-May 2020) of the pandemic. Path models allowed for the examination of PRS and previously identified COVID-19 impact constructs. Results: There was a main effect of the AUD PRS on AUD symptoms within the EA group (ß: .165, p < .01). Additionally, food/housing insecurity was predictive in the AMER group (ß.295, p < .05), and greater increases in substance use were associated with AUD symptoms for EA (ß:.459, p < .001) and AMER groups (ß:.468, p < .001). Conclusions: Greater food/housing instability and increases in substance use, as well higher scores on PRS are associated with more AUD symptoms for some ancestral groups within this college sample.

A 6-year-old boy with an atypical liver neoplasm harboring a novel RPS6KA3 variant.

Pediatric hepatoblastoma (HBL) and hepatocellular carcinoma (HCC) are primary liver malignant neoplasms with 5-year event-free survival of >80% and <30%, respectively. In these patients, α-fetoprotein levels can guide surgical intervention and monitor disease progression. Although histology and immunohistochemical stains support diagnosis, genetic testing can elucidate mechanisms that drive pathogenesis. Pediatric HBL and HCC harbor well-characterized molecular signatures such as alterations in CTNNB1, TERT, and AXIN1 that alter the Wnt/ß-catenin pathway. Approximately 8% of individuals with HCC harbor RPS6KA3 variants that appear with other gene mutations. Herein, we report a novel solitary pathogenic RPS6KA3 variant finding in a 6-year-old boy whose final diagnosis was hepatocellular malignant neoplasm, not otherwise specified.

Dynamic Multi-Mode Mie Model for Gain-Assisted Metal Nano-Spheres.

Coupling externally pumped gain materials with plasmonic spherical particles, even in the simplest case of a single spherical nanoparticle in a uniform gain medium, generates an incredibly rich variety of electrodynamic phenomena. The appropriate theoretical description of these systems is dictated by the quantity of the included gain and the size of the nano-particle. On the one hand, when the gain level is below the threshold separating the absorption and the emission regime, a steady-state approach is a rather adequate depiction, yet a time dynamic approach becomes fundamental when this threshold is exceeded. On the other hand, while a quasi-static approximation can be used to model nanoparticles when they are much smaller than the exciting wavelength, a more complete scattering theory is necessary to discuss larger nanoparticles. In this paper, we describe a novel method including a time-dynamical approach to the Mie scattering theory, which is able to account for all the most enticing aspects of the problem without any limitation in the particle's size. Ultimately, although the presented approach does not fully describe the emission regime yet, it does allow us to predict the transient states preceding emission and represents an essential step forward in the direction of a model able to adequately describe the full electromagnetic phenomenology of these systems.

A statistical genetic investigation of psychiatric resilience.

Background: Although trauma exposure (TE) is a transdiagnostic risk factor for many psychiatric disorders, not everyone who experiences TE develops a psychiatric disorder. Resilience may explain this heterogeneity; thus, it is critical to understand the etiologic underpinnings of resilience.Objective: The present study sought to examine the genetic underpinnings of psychiatric resilience using genome-wide association studies (GWAS), genome-wide complex trait analysis (GCTA), and polygenic risk score (PRS) analyses.Method: Participants were 6,634 trauma exposed college students attending a diverse, public university in the Mid Atlantic. GWAS and GCTA analyses were conducted, and using GWAS summary statistics from large genetic consortia, PRS analyses examined the shared genetic risk between resilience and various phenotypes.Results: Results demonstrate that nine single-nucleotide polymorphisms (SNPs) met the suggestive of significance threshold, heritability estimates for resilience were non-significant, and that there is genetic overlap between resilience and AD, as well as resilience and PTSD.Conclusion: Mixed findings from the present study suggest additional research to elucidate the etiological underpinnings of resilience, ideally with larger samples less biased by variables such as heterogeneity (i.e. clinical vs. population based) and population stratification. Genetic investigations of resilience have the potential to elucidate the molecular bases of stress-related psychopathology, suggesting new avenues for prevention and intervention efforts.

Resilience may explain the heterogeneity in outcomes following trauma exposure; thus, it is critical to understand the etiologic underpinnings of resilience.The present study sought to examine the genetic underpinnings of psychiatric resilience using genome-wide association studies (GWAS), genome-wide complex trait analysis (GCTA), and polygenic risk score (PRS) analyses.Results demonstrated shared genetic overlap between resilience and Alcohol Dependence, as well as resilience and PTSD.Genetic investigations of resilience have the potential to elucidate the molecular bases of stress-related psychopathology, suggesting new avenues for prevention and intervention efforts.

Genetic associations between alcohol phenotypes and life satisfaction: a genomic structural equation modelling approach.

Alcohol use (i.e., quantity, frequency) and alcohol use disorder (AUD) are common, associated with adverse outcomes, and genetically-influenced. Genome-wide association studies (GWAS) identified genetic loci associated with both. AUD is positively genetically associated with psychopathology, while alcohol use (e.g., drinks per week) is negatively associated or NS related to psychopathology. We wanted to test if these genetic associations extended to life satisfaction, as there is an interest in understanding the associations between psychopathology-related traits and constructs that are not just the absence of psychopathology, but positive outcomes (e.g., well-being variables). Thus, we used Genomic Structural Equation Modeling (gSEM) to analyze summary-level genomic data (i.e., effects of genetic variants on constructs of interest) from large-scale GWAS of European ancestry individuals. Results suggest that the best-fitting model is a Bifactor Model, in which unique alcohol use, unique AUD, and common alcohol factors are extracted. The genetic correlation (rg) between life satisfaction-AUD specific factor was near zero, the rg with the alcohol use specific factor was positive and significant, and the rg with the common alcohol factor was negative and significant. Findings indicate that life satisfaction shares genetic etiology with typical alcohol use and life dissatisfaction shares genetic etiology with heavy alcohol use.

Is pre-college interpersonal trauma associated with cannabis use?

OBJECTIVE: To examine the prevalence and correlates of lifetime cannabis use (i.e., experimental [use 1-5 times] and non-experimental [use ≥ 6 times]) in relation to interpersonal trauma (IPT) above and beyond relevant covariates. PARTICIPANTS: A large (n = 9,889) representative sample of college students at an urban university in the southeastern part of the United States. METHODS: Participants were 4 cohorts of first-year college students who completed measures of demographics, cannabis, alcohol, nicotine, and IPT. Associations were estimated using multinomial logistic regressions. RESULTS: The prevalence of lifetime cannabis use was 28.1% and 17.4% for non-experimental and experimental cannabis use, respectively. IPT was significantly associated with experimental and non-experimental cannabis use above and beyond effects of sex, race, cohort, alcohol, and nicotine. CONCLUSIONS: Results show that cannabis use is prevalent among college students and is associated with IPT above and beyond associations with sex, race, and other substance use.

First Description of the Nuclear and Mitochondrial Genomes and Associated Host Preference of Trichopoda pennipes, a Parasitoid of Nezara viridula.

Trichopoda pennipes is a tachinid parasitoid of several significant heteropteran agricultural pests, including the southern green stink bug, Nezara viridula, and leaf-footed bug, Leptoglossus phyllopus. To be used successfully as a biological control agent, the fly must selectively parasitize the target host species. Differences in the host preference of T. pennipes were assessed by assembling the nuclear and mitochondrial genomes of 38 flies reared from field-collected N. viridula and L. phyllopus. High-quality de novo draft genomes of T. pennipes were assembled using long-read sequencing. The assembly totaled 672 MB distributed among 561 contigs, having an N50 of 11.9 MB and a GC of 31.7%, with the longest contig at 28 MB. The genome was assessed for completeness using BUSCO in the Insecta dataset, resulting in a score of 99.4%, and 97.4% of the genes were single copy-loci. The mitochondrial genomes of the 38 T. pennipes flies were sequenced and compared to identify possible host-determined sibling species. The assembled circular genomes ranged from 15,345 bp to 16,390 bp and encode 22 tRNAs, two rRNAs, and 13 protein-coding genes (PCGs). There were no differences in the architecture of these genomes. Phylogenetic analyses using sequence information from 13 PCGs and the two rRNAs individually or as a combined dataset resolved the parasitoids into two distinct lineages: T. pennipes that parasitized both N. viridula and L. phyllopus, and others that parasitized only L. phyllopus.

Adherence to Inhalation Devices in Patients with Chronic Obstructive Pulmonary Disease.

Purpose: Chronic obstructive pulmonary disease (COPD) affects millions of people around the world. Poor adherence to treatment contributes to increased severity of symptoms, morbidity, and mortality. The objective of this study was to establish the adherence of patients diagnosed with COPD by their devices for inhalation in a group of patients, Colombia. Patients and Methods: This was a cross-sectional study of patients treated in the Colombian health system. Adherence to inhalation devices was evaluated with the TAI-10 instrument (Inhaler Adherence Test). A score of 50 points was considered good adherence. Results: A total of 500 patients from 84 cities were identified, with a median age of 79.0 years, and 59.2% were women. A total of 45% had GOLD B COPD, and 56.6% had good adherence. Average adherence was 47.4±5.3 points, and no significant differences were found according to inhalation devices (p=0.949). Training performed by specialist physicians (OR: 1.75; 95% CI: 1.17-2.62), use of an inhaler for less than 1 year (OR: 1.59; 95% CI: 1.04-2.43), use of short-acting ß2-adrenergic agonists (OR: 1.58; 95% CI: 1.05-2.38) and increased satisfaction with the inhalation device (OR: 1.09; 95% CI: 1.04-1.14) were associated with good adherence, while those from the central region (OR: 0.55; 95% CI: 0.36-0.83), who had a COPD evolution time of less than 5 years (OR: 0.57; 95% CI: 0.37-0.98) and had diabetes mellitus (OR: 0.60; 95% CI: 0.37-0.98) had lower adherence. Conclusion: Adherence to treatment with inhaled bronchodilators and glucocorticoids were not very high, with no significant differences by type of inhalation device. Satisfaction and training by specialists increased adherence.

Alcohol use and alcohol use disorder differ in their genetic relationships with PTSD: A genomic structural equation modelling approach.

PURPOSE: Posttraumatic Stress Disorder (PTSD) is associated with increased alcohol use and alcohol use disorder (AUD), which are all moderately heritable. Studies suggest the genetic association between PTSD and alcohol use differs from that of PTSD and AUD, but further analysis is needed. BASIC PROCEDURES: We used genomic Structural Equation Modeling (genomicSEM) to analyze summary statistics from large-scale genome-wide association studies (GWAS) of European Ancestry participants to investigate the genetic relationships between PTSD (both diagnosis and re-experiencing symptom severity) and a range of alcohol use and AUD phenotypes. MAIN FINDINGS: When we differentiated genetic factors for alcohol use and AUD we observed improved model fit relative to models with all alcohol-related indicators loading onto a single factor. The genetic correlations (rG) of PTSD were quite discrepant for the alcohol use and AUD factors. This was true when modeled as a three-correlated-factor model (PTSD-AUD rG:.36, p < .001; PTSD-alcohol use rG: -0.17, p < .001) and as a Bifactor model, in which the common and unique portions of alcohol phenotypes were pulled out into an AUD-specific factor (rG with PTSD:.40, p < .001), AU-specific factor (rG with PTSD: -0.57, p < .001), and a common alcohol factor (rG with PTSD:.16, NS). PRINCIPAL CONCLUSIONS: These results indicate the genetic architecture of alcohol use and AUD are differentially associated with PTSD. When the portions of variance unique to alcohol use and AUD are extracted, their genetic associations with PTSD vary substantially, suggesting different genetic architectures of alcohol phenotypes in people with PTSD.

Precollege and New-Onset College Interpersonal Trauma as Predictors of Baseline and Changes in Alcohol Use Disorder Symptoms During College.

College is a high-risk time for interpersonal trauma (IPT) exposure (e.g., physical or sexual abuse/assault), a potent form of trauma exposure. College is also a high-risk time for alcohol misuse, as use begins and increases in adolescence and peaks in the early/mid-20s. In addition, although IPT is associated with alcohol misuse, less clear is whether distal (prior to college) or proximal (during college) IPT impacts alcohol use disorder (AUD) symptoms at the beginning of college and/or changes in symptoms during college. Data were collected from a large, longitudinal study of college students, attending a large public university in the southeast, who had reported lifetime IPT as well as lifetime alcohol use. Participants in the current study were 18.5 years old (SD = 0.46), primarily female (67.2%), and of diverse racial backgrounds (e.g., 53.4% White, 18.5% Black, 12.7% Asian, 15.4% Other). Latent change score analyses were employed to test the impact of IPT prior to college and IPT during college on initial levels of, and changes in, AUD symptoms during college. Those who experienced an IPT prior to college reported more AUD symptoms at the beginning of college and less changes in AUD symptoms during the first year of college. Those who experienced an IPT in the first 2 and last 2 years of college reported greater increases in symptoms in the first 2 and last 2 years of college, respectively. Findings suggest that prevention and intervention efforts for those who experience an IPT prior to or during college may be useful in reducing AUD symptoms during that time period.

Foot plantar soft tissue malignant myoepithelioma tumor: Case report and review of the literature.

The spectrum of myoepithelial tumors usually occur in the salivary glands, and occasionally in the skin, breast, upper aero-digestive tract, and soft tissues. The myoepithelial tumors have no sex predominance and usually present within a wide range of age of distribution around the third and fifth decades. We describe a 12 year old male patient with primary malignant myoepithelial tumor in the foot plantar soft tissues. Including this tumor with unusual location, and age of presentation is essential in the differential diagnosis for soft tissue tumors in the pediatric population.