School Psychology Supervisors' Perceptions of Specialist-Level Training: An Exploratory Study.

Surveys of trainers in school psychology have been administered to examine training competencies and content delivered to school psychology trainees. Surveys of practitioners working with school psychology trainees are limited as discussed by Lewis et al. (2005). The purpose of this exploratory study is to seek to understand the perceptions of specialist-level site-based supervisors in relation to practicum students' knowledge in several competency areas. Utilizing the National Association of School Psychologists' Model for Comprehensive and Integrated School Psychological Services and Standards for Graduate Preparation of School Psychologists as reported by NASP (2020b) and commonly reported school psychology practices as discussed by McNamara et al. (2019), a survey was developed and administered to specialist-level practicum supervisors. Results of Chronbach's alpha analyses examining internal consistency for each of the seven domains ranged from good to excellent (0.85-0.95) although mean differences in domain ratings were not found to be significant. Results of the study are presented along with study limitations and directions for future research.

GDF15 Induces Anorexia through Nausea and Emesis.

Growth differentiation factor 15 (GDF15) is a cytokine that reduces food intake through activation of hindbrain GFRAL-RET receptors and has become a keen target of interest for anti-obesity therapies. Elevated endogenous GDF15 is associated with energy balance disturbances, cancer progression, chemotherapy-induced anorexia, and morning sickness. We hypothesized that GDF15 causes emesis and that its anorectic effects are related to this function. Here, we examined feeding and emesis and/or emetic-like behaviors in three different mammalian laboratory species to help elucidate the role of GDF15 in these behaviors. Data show that GDF15 causes emesis in Suncus murinus (musk shrews) and induces behaviors indicative of nausea/malaise (e.g., anorexia and pica) in non-emetic species, including mice and lean or obese rats. We also present data in mice suggesting that GDF15 contributes to chemotherapy-induced malaise. Together, these results indicate that GDF15 triggers anorexia through the induction of nausea and/or by engaging emetic neurocircuitry.

Adult child caregiver health trajectories and the impact of multiple roles over time.

Guided by stress process and life course theory, the purpose of this study was to examine adult child caregivers' psychological and physical health trajectories and how their multiple family (caregiving, marital, and parenting) and nonfamily (employment) roles contributed to these health outcomes over time. Seven waves of data from the Health and Retirement Study were analyzed for 1,300 adult child caregivers using latent growth curve models. Adult child caregivers have distinct psychological and physical health trajectories that are related to their roles over time. The importance of any given role varies by the type of health outcome and timing in the life course. Caregiving alone does not contribute to adult child caregivers' psychological and physical health; marital and employment roles also contribute significantly to caregivers' life courses.

Effects of glucocorticoid exposure on growth and structural maturation of the heart of the preterm piglet.

Inadequate maintenance of systemic blood flow in neonates following preterm birth is associated with increased morbidity and mortality, and may be due in part to structural immaturity of the myocardium. Maternal glucocorticoid administration is associated with improved cardiovascular function, and possibly promotes structural maturation of the myocardium. This study assessed the structural maturity of the myocardium in male and female preterm and term piglets, and preterm piglets exposed to a regimen of maternal glucocorticoids as used clinically. In preterm, term and glucocorticoid exposed preterm piglets cardiomyocyte maturity was examined by measuring the proportion of binucleated myocytes and the volumes of single living ventricular cardiomyocytes with fluorescence microscopy. Ventricular apoptosis and proliferation were measured by immunohistochemistry. Preterm piglet hearts had fewer binucleated myocytes, smaller myocytes, and more proliferative and fewer apoptotic nuclei than term hearts. Maternal glucocorticoid treatment resulted in increased binucleation with no increase in myocyte volume, and levels of proliferation and apoptosis that were more similar to the term heart. Atrial weights were increased and in female piglets there was an increase in the ratio of left to right ventricular weight. The observed changes in atrial mass and myocyte structural maturation correlated with changes in cardiac function of isolated hearts of littermates. In conclusion, the association between increased myocardial maturation following glucocorticoid exposure, improved cardiac function in littermates, and clinical improvement in human neonatal cardiac function exposed to antenatal glucocorticoids, suggests that glucocorticoid exposure contributes to improved cardiovascular function in preterm infants by promoting myocardial structural maturity.

Feature-positive and feature-negative learning in honey bees.

Honey bees (Apis mellifera anatolica) were subjected to sequential trials where they were given the choice between a feature-positive and a feature-negative feeding plate. The 'feature' being manipulated is the presence of a single blue circle among three circles marking the location of a small sucrose reward. That is, a 'feature-negative' target had three white circles, while a 'feature-positive' target had two white circles and one blue one. Two experiments were performed. In both experiments, each bee was tested under two different reward scenarios (treatments). In the first experiment, during the feature-positive treatment bees received 4 µl of 2 mol l(-1) sucrose when choosing the feature-positive plate, but received 4 µl of saturated NaCl solution (saltwater) when choosing the feature-negative plate. During the feature-negative treatment, bees were rewarded when visiting the feature-negative plate, while visitation to the feature-positive plate only offered bees the saltwater. The second experiment was a repeat of the first except that pure water was offered instead of saltwater in the non-rewarding feeding plate. As an experimental control, a set of bees was offered sequential trials where both the feature-positive and feature-negative plates offered the sucrose reward. Bee feeding plate choice differed between the feature-positive and feature-negative treatments in both experiments. Bees favored the feeding plate type with the sucrose reward in each treatment, and never consumed the saltwater or pure water when encountered in either treatment. Further, behavior of bees during both the feature-positive and feature-negative treatments differed from that of control bees. However, neither feature-positive nor feature-negative learning reached high levels of success. Further, a feature-positive effect was seen when pure water was offered; bees learned to solve the feature-positive problem more rapidly. When we tested bees using simply the choice of blue versus white targets, where one color held the sucrose reward and the other the saltwater, a bee's fidelity to the color offering the sucrose reward quickly reached very high levels.

A replication of the 5-7 day dream-lag effect with comparison of dreams to future events as control for baseline matching.

The dream-lag effect refers to there being, after the frequent incorporation of memory elements from the previous day into dreams (the day-residue), a lower incorporation of memory elements from 2 to 4 days before the dream, but then an increased incorporation of memory elements from 5 to 7 days before the dream. Participants (n=8, all female) kept a daily diary and a dream diary for 14 days and then rated the level of matching between every dream report and every daily diary record. Baseline matching was assessed by comparing all dream reports to all diary records for days that occurred after the dream. A significant dream-lag effect for the 5-7 day period, compared to baseline and compared to the 2-4 day period, was found. This may indicate a memory processing function for sleep, which the dream content may reflect. Participants' and three independent judges' mean ratings also confirmed a significant day-residue effect.

Expression of multiple glutamate transporter splice variants in the rodent testis.

Glutamate is a regulated molecule in the mammalian testis. Extracellular regulation of glutamate in the body is determined largely by the expression of plasmalemmal glutamate transporters. We have examined by PCR, western blotting and immunocytochemistry the expression of a panel of sodium-dependent plasmalemmal glutamate transporters in the rat testis. Proteins examined included: glutamate aspartate transporter (GLAST), glutamate transporter 1 (GLT1), excitatory amino acid carrier 1 (EAAC1), excitatory amino acid transporter 4 (EAAT4) and EAAT5. We demonstrate that many of the glutamate transporters in the testis are alternately spliced. GLAST is present as exon-3- and exon-9-skipping forms. GLT1 was similarly present as the alternately spliced forms GLT1b and GLT1c, whereas the abundant brain form (GLT1a) was detectable only at the mRNA level. EAAT5 was also strongly expressed, whereas EAAC1 and EAAT4 were absent. These patterns of expression were compared with the patterns of endogenous glutamate localization and with patterns of d-aspartate accumulation, as assessed by immunocytochemistry. The presence of multiple glutamate transporters in the testis, including unusually spliced forms, suggests that glutamate homeostasis may be critical in this organ. The apparent presence of many of these transporters in the testis and sperm may indicate a need for glutamate transport by such cells.

Human sulfotransferases and their role in chemical metabolism.

Sulfonation is an important reaction in the metabolism of numerous xenobiotics, drugs, and endogenous compounds. A supergene family of enzymes called sulfotransferases (SULTs) catalyze this reaction. In most cases, the addition of a sulfonate moiety to a compound increases its water solubility and decreases its biological activity. However, many of these enzymes are also capable of bioactivating procarcinogens to reactive electrophiles. In humans three SULT families, SULT1, SULT2, and SULT4, have been identified that contain at least thirteen distinct members. SULTs have a wide tissue distribution and act as a major detoxification enzyme system in adult and the developing human fetus. Nine crystal structures of human cytosolic SULTs have now been determined, and together with site-directed mutagenesis experiments and molecular modeling, we are now beginning to understand the factors that govern distinct but overlapping substrate specificities. These studies have also provided insight into the enzyme kinetics and inhibition characteristics of these enzymes. The regulation of human SULTs remains as one of the least explored areas of research in the field, though there have been some recent advances on the molecular transcription mechanism controlling the individual SULT promoters. Interindividual variation in sulfonation capacity may be important in determining an individual's response to xenobiotics, and recent studies have begun to suggest roles for SULT polymorphism in disease susceptibility. This review aims to provide a summary of our present understanding of the function of human cytosolic sulfotransferases.

Active site mutations and substrate inhibition in human sulfotransferase 1A1 and 1A3.

Human SULT1A1 is primarily responsible for sulfonation of xenobiotics, including the activation of promutagens, and it has been implicated in several forms of cancer. Human SULT1A3 has been shown to be the major sulfotransferase that sulfonates dopamine. These two enzymes shares 93% amino acid sequence identity and have distinct but overlapping substrate preferences. The resolution of the crystal structures of these two enzymes has enabled us to elucidate the mechanisms controlling their substrate preferences and inhibition. The presence of two p-nitrophenol (pNP) molecules in the crystal structure of SULT1A1 was postulated to explain cooperativity at low and inhibition at high substrate concentrations, respectively. In SULT1A1, substrate inhibition occurs with pNP as the substrate but not with dopamine. For SULT1A3, substrate inhibition is found for dopamine but not with pNP. We investigated how substrate inhibition occurs in these two enzymes using molecular modeling, site-directed mutagenesis, and kinetic analysis. The results show that residue Phe-247 of SULT1A1, which interacts with both p-nitrophenol molecules in the active site, is important for substrate inhibition. Mutation of phenylalanine to leucine at this position in SULT1A1 results in substrate inhibition by dopamine. We also propose, based on modeling and kinetic studies, that substrate inhibition by dopamine in SULT1A3 is caused by binding of two dopamine molecules in the active site.

Structure of a human carcinogen-converting enzyme, SULT1A1. Structural and kinetic implications of substrate inhibition.

Sulfonation catalyzed by sulfotransferase enzymes plays an important role in chemical defense mechanisms against various xenobiotics but also bioactivates carcinogens. A major human sulfotransferase, SULT1A1, metabolizes and/or bioactivates many endogenous compounds and is implicated in a range of cancers because of its ability to modify diverse promutagen and procarcinogen xenobiotics. The crystal structure of human SULT1A1 reported here is the first sulfotransferase structure complexed with a xenobiotic substrate. An unexpected finding is that the enzyme accommodates not one but two molecules of the xenobiotic model substrate p-nitrophenol in the active site. This result is supported by kinetic data for SULT1A1 that show substrate inhibition for this small xenobiotic. The extended active site of SULT1A1 is consistent with binding of diiodothyronine but cannot easily accommodate beta-estradiol, although both are known substrates. This observation, together with evidence for a disorder-order transition in SULT1A1, suggests that the active site is flexible and can adapt its architecture to accept diverse hydrophobic substrates with varying sizes, shapes and flexibility. Thus the crystal structure of SULT1A1 provides the molecular basis for substrate inhibition and reveals the first clues as to how the enzyme sulfonates a wide variety of lipophilic compounds.