Grant Program Research Articles

DEVELOPMENT OF THE NEXT ESSA RESEARCH STRATEGY

INTRODUCTION The generation and use of research is a function within ESSA and the first research strategy was developed for the period 2018 - 2021. Research program activities are diverse. ESSA has hosted the Research Committee and the Publications Committee for 5 years. ESSA has facilitated the development of member-driven Guidelines, Consensus and Position Statements for use by professionals in practice. ESSA has hosted an annual Research Grant Program and a biannual scientific conference. This paper outlines the research strategy development project. METHODS The previous strategy delivered research grants and ESSA publications. Investments were made into administration and research governance including release of the ESSA Research Publications Development Guideline. Consultation on the development of the next Research Strategy included presentations and surveys to engage members, key stakeholders and staff about: the program; the key strategy pillars; principles; and actions. Actions were assessed for feasibility and priority. RESULTS The outcomes of the consultation on the ESSA Research Strategy 2023-2026 identified four pillars of capacity building, engagement, translation and data, and research for policy and practice priorities. The use of research publications by ESSA accredited professionals and industry will be guided by a translation framework, aligning with the objectives of the National Health and Medical Research Council (NHMRC) Translation Strategy 2022-2025, the resources of the National Centre of Implementation Science and the ESSA Strategic Plan. This will support members to leverage research findings, to encourage researchers to develop translation collateral and to implement new research results. The strategy will have actions, references and tools to help accredited professionals to engage in research translation. CONCLUSIONS The Research Strategy and translation framework will be outlined. The paper will include examples relating to physical activity. ESSA’s next Research Strategy is to further support research generation and use by ESSA accredited professionals, staff and the industry.

Physical activity mitigates serotonin and oxidative stress-associated mesenteric arterial endothelial dysfunction in obesity

Introduction: Serotonin (5-HT) signaling may play a role in modulating vascular endothelial function. Obesity-induced oxidative stress causes the development of cardiovascular disease (CVD). We aimed to investigate the protective effect of voluntary wheel running (EX) on serotonin receptor (5-HT1B) and oxidative stress in the mesenteric artery of obese mice. Methods: Mice were randomly divided into four groups. They were fed a control low-fat diet (LF) or high-fat diet (HF; 45% of calories from fat) and provided with voluntary wheel running (LF-EX or HF-EX) or a sedentary condition. The protein expressions of phosphorylated-endothelial nitric oxide synthase (p-eNOS), 5-HT1B receptor, Akt, and proteins regulating oxidative stress were quantified by Western blot analysis. Statistical comparisons between groups were performed with two-way ANOVA with Fisher’s LSD test. Results: The protein expressions of p-eNOS, 5-HT1B receptor, and p-Akt in HF were lower compared to LF, but EX increased the protein levels ( P < 0.05). NOX2 in HF was higher compared to LF, but EX decreased it ( P < 0.05). SOD1, SOD2, and UCP2 in HF were lower compared to LF, but EX increased the protein levels ( P < 0.05). There was no difference in expressions of Akt, Gαq/11, NOX4, and VDUP1 between groups. Conclusion: Voluntary wheel running improves e-NOS-mediated vascular endothelial function possibly via increased 5-HT1B receptors and reduced oxidative stress, which could mitigate the risk of obesity-induced CVD. This study was supported by grants from the Cardiovascular Research Foundation Asia (#16215 to Y. P.) and the University of Houston (Small Grant Program to Y. P.). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Fibulin-5 Is Required for Small Artery Development and Function

Introduction: Fibulins are a family of eight extracellular matrix proteins with diverse functions. Fibulin-4 and -5 (FBLN-4 and -5), in particular, have been shown to be important for elastic fiber assembly. Mutations in each of the genes lead to cutis laxa, a syndrome characterized by loose skin with variable organ involvement, particularly in the vasculature, lungs and skeleton. We recently characterized a mouse model carrying a disease-causing mutation in Fbln4 (E57K) and, contrary to conduit arteries that had elastic fiber fragmentation and stiffness, Fbln4E57K resistance arteries were structurally intact. Functionally however, Fbln4E57K mesenteric arteries exhibited endothelial dysfunction secondary to increased shear stress from large artery stiffness. Loss of FBLN5 has been shown to lead to elastic fiber fragmentation in conduit arteries, but the consequences of its loss on resistance arteries are unknown. Therefore, the objectives of this study were to determine the structural and functional consequences of FBLN5 loss on resistance arteries. Methods: We utilized adult Fbln5 knock-out (KO) mice and examined the ultrastructure of renal and mesenteric arteries via transmission electron microscopy. Functionally, using pressure myography, we characterized the myogenic tone and reactivity of Fbln5 KO and littermate control third-order mesenteric arteries to various vasoactive substances including acetylcholine, papaverine, angiotensin II, phenylephrine and potassium chloride. Results: While the internal elastic lamina (IEL) of Fbln5KO mice resistance arteries was largely intact, the external elastic lamina (EEL) was nearly absent. Similar to Fbln4E57K mice, Fbln5KO mesenteric arteries exhibited impaired endothelial-dependent vasorelaxation, likely secondary to proximal large artery stiffness. Unlike Fbln4E57K mesenteric arteries however, Fbln5 KO mesenteric arteries exhibited increased myogenic tone as well as a hypercontractile response to angiotensin II and potassium chloride, but not to phenylephrine. Conclusions: In addition to highlighting differences in the requirements for elastic fiber assembly along the arterial tree, these data emphasize the differential contribution of FBLN4 and FBLN5 to IEL vs. EEL in resistance arteries and suggest pathway-specific changes in smooth muscle cell contractility secondary to FBLN5 deficiency. This work was supported by the Washington University Pediatric Nephrology Research Core Pilot Grant Program to CMH. Funds were also provided by The Department of Pediatrics at Washington University in St. Louis School of Medicine to CMH. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

ASA Mentoring Grant Program: Then and Now

ASA Mentoring Grant Program: Then and Now

Loss of Pnn in neurons regulates protein expression of genes involved in frontotemporal dementia and alters locomotor activities in mice

The regulation of pre-mRNA alternative splicing in neurons is considered to be associated with neurodegeneration disease. In the present study, we applied an inducible neuron-specific gene depletion mouse model to determine whether the expression of Pnn, a mRNA splicing regulator, is involved in the induction of neurodegeneration. Six-weeks old male mice carrying CaMKII-CreERT2 gene cassette and Pnnflox/flox allele were injected with tamoxifen to induce the disruption of Pnn gene structure. In addition to histopathological and biochemical examination, brain MRI analysis and the observation on behavior alteration were also performed on mice with neuronal Pnn depletion. Locomotor activity measurement showed that the travel distance, ratio of moving/resting, central time, and central distance in neuronal Pnn-depleted mice were all higher than that in wild type mice since three months after induction of Pnn gene disruption. Moreover, the decrease in gripping force was observed in mice with neuronal Pnn depletion. MRI analysis further demonstrated that loss of Pnn in neurons leads to cerebral ventricular dilatation and hippocampal atrophy in 10-month-old mice. Mass spectrometry-based immuno-precipitation proteomics indicated the interaction between Pnn and frontotemporal dementia (FTD)-associated proteins, including TDP-43, FUS, and hnRNPA1. It is worth noting that both immunofluorescent stainings and Western blottings demonstrated the up-regulation of FTD-associated proteins in hippocampus and cerebral cortex of mice with neuronal Pnn depletion. However, the transcriptional level of genes involved in FTD were not altered by Pnn depletion. In conclusion, loss of Pnn in neurons leads to behavioral alteration in mice with regulating protein expression of genes involved in FTD, implying the involvement of Pnn deficiency in neurodegeneration. This research was supported by Chang Gung Medical Research Program Grant (Grant number: CMRPG 8N0341-2). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

NFAT5 upregulates osmolyte transporters to protect IMCD3 cells against hyperosmolarity

The kidney inner medulla is one of the only places in the body exposed to extremely high osmolarity, reaching up to 1300 mOsm, while the iso-osmotic cortex and plasma are ≍300m mOsm. Renal epithelial cells need a mechanism to address the stress that comes with hyperosmolarity. One possible mechanism is regulation of osmolyte transporters to increase intracellular osmolyte concentration and reduce osmotic stress. NFAT5 is an important factor in regulating renal epithelial cell responses to high osmolarity. We hypothesize that NFAT5 is protective in inner medullary collecting duct cells (IMCD3) via upregulation of key transporters. To test this hypothesis, we used CRISPR to delete NFAT5 in IMCD3 cells. IMCD3 -NFAT5 null (NFAT5 null) and control (Ctl, IMCD3) cells were used and cell death assessed. Cells were plated at the same concentrations, in media (320mmol) with additional osmolarities of: urea (160mmol), mannitol (160mmol) and salt (40 and 80 mmol). Cell death was measured over 5 days using Janus Green B, which permeates living cell membranes. Cells were incubated with Janus Green B, lysed and then absorbance measured with a spectrophotometer to determine concentration. Data were analyzed as mean ± SEM; cell confluence, two-way ANOVA, n=3-5. Total mRNA was also isolated for qPCR analysis and data expressed as a fold change (DCT) over housekeeping (PPIA). At iso-osmolarity (»300mOsm), no differences were observed between NFAT5 null and Ctl cells. However, by day 3, NFAT5 null cells had reduced cell growth in all hyperosmolar conditions: urea 160 mmol (1.192 ± 0.225 vs. 1.953 ± 0.167 Wt ****p<0.0001, n=4), mannitol 160 mmol (0.852 ± 0.135 vs. 1.683 ± 0.283 Wt ****p<0.0001, n=3-4), NaCl 40 mmol (1.745 ± 0.210 vs. 2.020 ± 0.252 Wt ****p<0.0001, n=4-5), NaCl 80 mmol (0.385 ± 0.059 vs. 1.089 ± 0.191 Wt ****p<0.0001, n=4-5). Interestingly, NFAT5 null cells recovered growth patterns similar to Ctl cells by day 5. This suggests that although NFAT5 is essential in the cellular response hyperosmolarity, other mechanisms are present that allow for adaptation over time. To address a possible mechanism, we performed qPCR investigating common osmo-protective genes. We hypothesized that expression is lower in the NFAT5 null cells as compared to Wt. When cultured with 40 mmol of NaCl (n=2), we found that the NFAT5 null cells showed a 3.31 fold reduction for SMIT1, a 2924.98 fold reduction for TauT, and a 4.91 fold reduction for BGT1 as compared to Wt, each of which are osmolyte transporters. Additionally, we saw a 161.46 fold reduction for AQP1, a water channel and a 4.91 fold reduction for Akr1b3, which influences water homeostasis, as compared to Wt. Together, these results suggest that NFAT5 is a critical regulator of both osmolyte and transporters. Here, we show that loss of NFAT5 reduces IMCD cell viability in the face of hyperosmotic stress, possibly through a reduction in key osmolyte transporters. These data suggest that NFAT5 is key in the renal epithelial cell response to, and survival in, the hyperosmolar environment of the inner medulla. Undergraduate Research Opportunity Program grant NIH NIDDK DK115660-01A1 University of Utah DOIM, UCares. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Neuromodulatory co-expression in cardiac vagal motor neurons of the Dorsal Motor Nucleus of the Vagus

Dorsal Motor Nucleus of the Vagus (DMV) activity is required for cardioprotection from physiological interventions such as remote ischemic pre-conditioning (RIPC). Herein, we discover the transcriptomic phenotypes of cardioprotective DMV neurons, by combining high throughput transcriptomics, 3D anatomical mapping, and neural tracing in 12 week old male and female Sprague Dawley rats. We find that DMV neurons appear to participate in neuromodulatory co-expression, including those that project to the heart. To distinguish potential mechanisms of cardioprotection, we highlight the functional significance of several transcripts in cardiac-projecting DMV neurons and we begin to validate these findings at the protein level. In our sc-RNAseq data we find that Snca (α-synuclein), the cardioprotective neuromodulator Adcyap1 (PACAP), and the neuropeptide Cartpt (CART) are enriched in cardiac-projecting DMV neurons. To contrast our molecular findings in cardioprotective DMV neurons, we have also collected single neuron HT-RTqPCR data from the other source of cardiac vagal motoneurons, the Nucleus Ambiguus (NA). Catecholaminergic transcripts, including Slc18a2 (VMAT2), Ddc, and Th, are enriched in cardiac-projecting DMV neurons relative to those of the NA. These findings implicate catecholaminergic processes, synuclein, and these secreted neuropeptides in cardioprotection. At the protein level, we found PACAP, CART, SNCA and TH enrichment, as well as co-localization of PACAP, TH, and ChAT, in cardiac-projecting DMV neurons. There is consistency between our findings from three spatial transcriptomics techniques and across sexes. Based on these results, we propose a 3D anatomical and molecular map of cardiac vagal motoneurons. This work fills a major gap in the understanding of the cellular mechanisms by which parasympathetic drive provides cardioprotection and provides a future translational path to emulating the positive vagal neuromodulatory effects on heart health. Funding was provided by the R01 HL161696 grant through National Heart, Lung, and Blood institute and the National Institutes of Health Common Fund SPARC Program Grant OT2OD030534. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Activation of PACAP+ vagal motoneurons following remote ischemic pre-conditioning

The Dorsal Motor Nucleus of the Vagus nerve (DMV) provides parasympathetic innervation of the intrinsic cardiac nervous system (ICN), and it has been shown that DMV activity is required for the cardioprotection induced by remote ischemic pre-conditioning (RIPC) against the pathological effects of myocardial infarction. However, the mechanism behind the DMV’s cardioprotective effects is not well understood. Previous literature has shown that the DMV and the other vagal motor nuclei, the nucleus ambiguus (NA), innervate distinct cells within the ICN. DMV neurons project to many other organs in addition to the heart. The cardioprotective neuropeptide Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) has been found to be expressed in the fibers innervating the ICN, where it is co-localized with the parasympathetic marker, ChAT. While we have found PACAP to be expressed in cardiac-projecting DMV neurons, it is unknown whether these neurons are preferentially activated in response to RIPC. To assess the activity of these neurons following RIPC, we performed immunofluorescence staining of brainstem tissue containing DMV neurons for both PACAP, and c-FOS, a neuronal activity-dependent marker. We hypothesized that PACAP+ DMV neurons would have increased activity following RIPC, and therefore increased c-FOS intensity and increased co-localization with PACAP compared to sham control. Our results suggest that PACAP+ neurons in the DMV show increased activity following RIPC compared to sham, as defined by increased c-FOS fluorescence intensity and co-localization with PACAP. These results suggest that PACAP+ neurons are activated during the cardioprotective response to remote ischemic pre-conditioning. Funding was provided by the R01 HL161696 grant through National Heart, Lung, and Blood institute and the National Institutes of Health Common Fund SPARC Program Grant OT2OD030534. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Spinal TNF-α receptor expression in a rodent model of respiratory motor neuron death

Intrapleural injection of cholera toxin B fragment conjugated to saporin (CTB-SAP) selectively kills respiratory motor neurons, and mimics aspects of neurodegenerative diseases including breathing deficits. In this model, phrenic long-term facilitation (pLTF) induced by acute intermittent hypoxia is enhanced following 7 days (d) of CTB-SAP vs. control rats, whereas pLTF in 28d CTB-SAP treated rats is comparable to pLTF in controls suggesting that the underlying mechanisms of plasticity at both time points differ. Inflammation is a hallmark of neurodegenerative diseases and is known to prevent pLTF. Furthermore, ketoprofen (NSAID) delivery attenuates pLTF in 7d CTB-SAP-treated rats, but enhances it in 28d CTB-SAP-treated rats; this suggests that inflammation contributes to pLTF in 7d CTB-SAP-treated rats, but undermines pLTF in 28d CTB-SAP-treated rats. In addition, cervical spinal inflammatory marker gene expression ( e.g., TNF-a) is increased in CTB-SAP rats, and pilot data suggest that soluble TNF receptor 1 (sTNFR1) inhibition differentially affects pLTF (Nichols and Smith , ibid). Thus, the goal of the current study is to investigate TNFR1 as a pharmacological target that can modulate inflammation to maximize pLTF and breathing in CTB-SAP rats. We hypothesized that C4 TNFR1 expression would be increased on phrenic motor neurons and glial cells of CTB-SAP rats vs. controls. To address this, we studied TNFR1 expression on phrenic motor neurons and glial cells using immunohistochemistry, confocal microscopy, and ImageJ analysis in male Sprague Dawley rats 7 and 28 days after intrapleural injection of: CTB-SAP or un-conjugated CTB and SAP (control); n=8/group. Our preliminary data (n=4/group) suggest that phrenic TNFR1 expression is increased in 7d CTB-SAP rats vs. controls (p<0.05), but is unaffected in 28d CTB-SAP rats vs. controls (p>0.05). Further data analysis is underway for phrenic as well as glial TNFR1 expression in CTB-SAP rats vs. controls. If C4 TNFR1 expression is increased, this would suggest that TNFR1 is a viable target for therapeutic intervention in CTB-SAP rats, and potentially in patients with breathing deficits due to respiratory motor neuron death. NSF Computational Neuroscience grant, MU CVM COR grant, and Spinal Cord Injury & Disease Research Program grant. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Cardiac Remodeling in Aged Rats after Early-life Chronic Stress: Sex-specific Outcomes and Associations with Metabolic Parameters

Cardiovascular disease is the leading cause of death worldwide. Additionally, the incidence of cardiovascular disease varies both across the lifespan and between sexes. While multiple factors influence the development and progression of cardiovascular pathology, prolonged stress is a prominent risk factor for adverse cardiac events. However, the interactions between stress, sex, and aging that impact cardiac susceptibility remain to be determined. To this end, we examined hypertrophy of the aged myocardium in a sex- and stress-specific manner. We hypothesized that sex and stress history would interact to predict cardiac outcomes and that susceptibility/resilience would associate with behavioral, endocrine, and metabolic parameters assessed across the lifespan. In this study, rats were either exposed to chronic variable stress (CVS) in late adolescence (n = 36/sex) or remained as unstressed controls (n = 24/sex). Rats were subsequently challenged with a forced swim test (FST) and glucose tolerance test (GTT) before ageing to 15 months. The FST and GTT were then repeated prior to tissue collection. Cardiac tissue was processed for histological analysis and quantification of ventricular morphology. The data indicated that early-life chronic stress had sex-specific consequences on the aged left ventricle as CVS females had greater concentric hypertrophy. Based on the level of inward remodeling, rats were then classified as susceptible or resilient. Multiple behavioral and endocrine factors in young and aged animals significantly interacted with hypertrophy, including coping behaviors and glucocorticoid responses to hyperglycemia. However, correlations with hypertrophy were only present in males. Male rats that were not exposed to CVS had a positive association between baseline corticosterone and hypertrophy. Alternatively, CVS males had a positive correlation between visceral adiposity and hypertrophy. Thus, sex-specific cardiac susceptibility/resilience relates to endocrine and metabolic measures depending on stress history. This outcome suggests that adverse experiences can have lasting impacts on homeostatic adaptation. Ultimately, these results highlight the importance of sex and prior stress exposure for disparities in cardiovascular risk. NIH R01 HL 150559 (B Myers) NIHH F30 OD032120 (C Dearing) Pilot Translation Research Program grant from the University of Cincinnati (B Myers). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Identifying associations of human surfactant protein A SNPs and allelic variants with retinopathy of prematurity

Retinopathy of prematurity (ROP) is the primary cause of childhood blindness worldwide. Previous studies showed that allelic single nucleotide polymorphic (SNP) variants of the human surfactant protein A genes (SP-A1, SP-A2) are associated with the development of respiratory distress syndrome and bronchopulmonary dysplasia (BPD). In this work, we hypothesized that SP-A SNPs and allelic variants are associated with altered risk of ROP in prematurely born infants. To test this hypothesis, we used a modified PCR-based method to detect variants of the SP-A1 and SP-A2 genes in a cohort of preterm infants. Infants born at <32 weeks’ gestation and/or<1500 grams were enrolled. Scavenged blood samples or cheek swabs were collected and DNA was extracted using the QIAamp DNA Mini Kit. We measured SNPs in SP-A1 and SP-A2 using Taqman probes for allelic discrimination by PCR or PCR/RFLP/sequencing method. Associations of SP-A1 and SP-A2 SNP allele frequencies with ROP and BPD were determined using chi-square and logistic regression analyses. Our results show that, of the total patient cohort (n=59), 42 patients had a BPD diagnosis (23 with ROP and 36 without ROP). DNA analysis of these samples identified associations of SP-A1 and SP-A2 SNPs and variants with ROP. For SP-A1, the following SNP associations were found for ROP using chi-square: rs1059047 (p=0.44), rs1136450 (p=0.63), rs1136451 (p=0.21), rs1059057 (p=0.52). For SP-A2, the following SNPs associations were identified with ROP: rs1059046 (p=0.51), rs17886395 (p=0.050), rs1965707 (p=0.031), rs1965708 (p=0.46). Logistic regression analysis indicated an association of ROP with the SP-A1 6A2 variant (p-value = 0.47, OR (6A2/*)=0.8036, 95%CI [0.2299 - 2.8082], OR (6A2/6A2) = 0.4327, 95%CI [0.1063 - 1.7615]), which conferred protection, as well as an association of ROP with SP-A2 6A2 (p-value = 0.0055) with decreased risk when 1A2 variant is present. We conclude that SP-A1/SP-A2 polymorphisms are associated with the presence of ROP in infants with BPD. The 6A4 SP-A1 and SP-A2 1A2 appear to confer protection in babies against ROP. Further studies will determine the mechanisms of this protective effect. Indiana University, University of Chicago Metcalf Internship Program Grant, The University of Oklahoma Health Sciences Center. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Pendampingan Penyusunan Proposal Program Kreativitas Mahasiswa (PKM) Prodi Manajemen Sekolah Tinggi Ilmu Ekonomi Bima

The PKM program is a routine grant program every year which will be participated in by PTN and PTS which is organized by the Belmawa Directorate as a forum for channeling student creative ideas. The hope is that by launching the Student Creativity Program (PKM) in various fields, it will train students to be able to present solutions to problems faced by the government, society, or the world of work/industry, so that the life of the nation and state moves in a better direction. The participation of students and accompanying lecturers in PKM activities can support the achievement of their higher education's IKU. Especially at IKU 1 (graduates get decent work), IKU 2 (students get experience outside campus), IKU 3 (lecturers carry out activities outside campus), and IKU 5 (the results of lecturers' work are used by the community). Apart from that, the output of this PKM program can be in the form of articles that are declared to have passed by reviewers and can be published in a scientific journal, which is a form of dissemination of activities carried out by students and indirectly contributes to progress and technology. However, the problem in 2024 is that there is still low student participation in taking part in PKM grants and low knowledge and understanding of students in preparing proposals and taking part in PKM and difficulty finding ideas to put into writing. The community service method uses a participatory method through a preliminary stage, core stage and advanced stage. The results of the activity show that it was carried out according to the timeline and increased student interest in developing ideas and skills as well as student interest in proposing PKM, this is proven by the increase in the number of PKM proposals proposed in the Simbelmawa system.

Perioada nord-americană

The purpose of this article is to bring to the forefront the theatrical activity carried out for eight years by Theodor-Cristian Popescu in the North American cultural landscape. Following the path of the Romanian theatre director, the article presents the performances he directed during his master’s degree at the University of Montana and also the theatrical events he staged in Montréal and Toronto, once he moved to Canada. Drawing on a variety of sources (press articles – reviews, interviews, press releases –, as well as program booklets, grant applications or evaluations of his teaching activity), the article aims to provide the Romanian public with a detailed presentation of Theodor-Cristian Popescu’s theatrical activity abroad (theatrical animator, director, teacher).

The selective serotonin reuptake inhibitor sertraline alters learning from aversive reinforcements in patients with depression: evidence from a randomized controlled trial.

Selective serotonin reuptake inhibitors (SSRIs) are first-line pharmacological treatments for depression and anxiety. However, little is known about how pharmacological action is related to cognitive and affective processes. Here, we examine whether specific reinforcement learning processes mediate the treatment effects of SSRIs. The PANDA trial was a multicentre, double-blind, randomized clinical trial in UK primary care comparing the SSRI sertraline with placebo for depression and anxiety. Participants (N = 655) performed an affective Go/NoGo task three times during the trial and computational models were used to infer reinforcement learning processes. There was poor task performance: only 54% of the task runs were informative, with more informative task runs in the placebo than in the active group. There was no evidence for the preregistered hypothesis that Pavlovian inhibition was affected by sertraline. Exploratory analyses revealed that in the sertraline group, early increases in Pavlovian inhibition were associated with improvements in depression after 12 weeks. Furthermore, sertraline increased how fast participants learned from losses and faster learning from losses was associated with more severe generalized anxiety symptoms. The study findings indicate a relationship between aversive reinforcement learning mechanisms and aspects of depression, anxiety, and SSRI treatment, but these relationships did not align with the initial hypotheses. Poor task performance limits the interpretability and likely generalizability of the findings, and highlights the critical importance of developing acceptable and reliable tasks for use in clinical studies. This article presents research supported by NIHR Program Grants for Applied Research (RP-PG-0610-10048), the NIHR BRC, and UCL, with additional support from IMPRS COMP2PSYCH (JM, QH) and a Wellcome Trust grant (QH).

Kids Run the Nation grants for youth running programs

Kids Run the Nation grants for youth running programs

College student transition program grants

College student transition program grants

Truist Financial launches new grant program

Truist Financial Corp. has announced the initial recipients of its Truist Community Catalyst Initiative, a three‐year program supporting local charitable efforts with statewide impact.

Innovative Finance and Asset Concessions Grant Program (DOT)

Innovative Finance and Asset Concessions Grant Program (DOT)

Mobilizing community-driven health promotion through community granting programs: a rapid systematic review.

Effective health promotion responds to the unique needs of communities. Community granting programs that fund community-driven health promotion initiatives are a potential mechanism to meet those unique needs. While numerous community health-focused programs are available, the various strategies used by granting programs to foster engagement, administer grants and support awardees have not been systematically evaluated. This rapid systematic review explores the administration of community granting programs and how various program components impact process and population health outcomes. A systematic search was conducted across three databases: Medline, SocINDEX, and Political Science Database. Single reviewers completed screening, consistent with a rapid review protocol. Studies describing or evaluating community granting programs for health or public health initiatives were included. Data regarding program characteristics were extracted and studies were evaluated for quality. A convergent integrated approach was used to analyze quantitative and qualitative findings. Thirty-five community granting programs, described in 36 studies, were included. Most were descriptive reports or qualitative studies conducted in the USA. Program support for grant awardees included technical assistance, workshops and training, program websites, and networking facilitation. While most programs reported on process outcomes, few reported on community or health outcomes; such outcomes were positive when reported. Programs reported that many funded projects were likely sustainable beyond program funding, due to the development of awardee skills, new partnerships, and securing additional funding. From the perspectives of program staff and awardees, facilitators included the technical assistance and workshops provided by the programs, networking amongst awardees, and the involvement of community members. Barriers included short timelines to develop proposals and allocate funds. This review provides a comprehensive overview of health-related community granting programs. Grant awardees benefit from technical assistance, workshops, and networking with other awardees. Project sustainability is enhanced by the development of new community partnerships and grant-writing training for awardees. Community granting programs can be a valuable strategy to drive community health, with several key elements that enhance community mobilization. PROSPERO #CRD42023399364.

243 Community-Campus Research Incubator (CCRI) Grant Program: 13 years of partnerships improving community health

OBJECTIVES/GOALS: With the knowledge that population health will not improve without including community voices in research, analysis of the UCI Institute for Clinical and Translational Science (ICTS) Community-Campus Research Incubator (CCRI) grants awarded since 2010 provides the foundation for understanding research partnerships impact on community health. METHODS/STUDY POPULATION: Over the past 13 years, the UCI ICTS CCRI program has funded 63 partnered research pilot or capacity-building projects, providing up to $30K annually to academic-community partnerships. Each year since 2010, between 3 and 7 projects were funded up to $5,000 annually for capacity-building activities and up to $10,000 annually for pilot research activities. Additionally, during the COVID-19 pandemic, a collaboration between the UCI ICTS and the local Healthcare Agency provided up to $20,000 to research partnership teams to study impact and interventions related to the pandemic, where 10 CCRI awards were given out. Evaluations of these research teams was completed at the end of the project, and at years 2 and 3 after the project ended. Analysis of the projects and partnerships aim to reveal the impact of these projects. RESULTS/ANTICIPATED RESULTS: In 2023, we compiled all evaluation data collected from 2010 – 2023 from the CCRI partnership grants, including traditional metrics of publications, subsequent grant applications submitted & awarded, presentations given, and return on investment for ICTS granted funds. Less traditional metrics include number of students trained, new tools or databases created, knowledge disseminated, and advances in clinical care. Since 2020, Translational Science Benefit Model metrics have been collected on community, policy, economic, and clinical domains. Since 2015, data on each CCRI partnership has been collected at the start and end of each project, with questions about attributes of each partner, trust, community engagement principles, and anticipated/actual impact of each project. DISCUSSION/SIGNIFICANCE: Organizing outcomes from the data collected will provide deep understanding of important components, functioning, and types and reach of partnered health research. This understanding will inform future action of the CCRI program in terms of what can be accomplished with a given amount of funding, and the constitution of successful partnerships.