Feasibility and Acceptability of a Physical Activity Group Program Using telerehabilitation during the COVID-19 Pandemic in Multiple early Intervention for Psychosis Services.

Background: Although physical activity (PA) is beneficial to young people with early psychosis (YEP) to improve physical health and psychiatric symptoms, few YEP initiate and maintain PA. The sports group interventions offered in early psychosis services had to be suspended due to the COVID-19 pandemic. Telehealth has shown promising results in different fields of health services including for patients with mental health disorders.

Lymphocytic Extracellular Signal-Regulated Kinase Dysregulation in Autism Spectrum Disorder.

Objective: Extracellular signal-regulated kinase (ERK1/2) is a conserved central intracellular signaling cascade involved in many aspects of neuronal development and plasticity. Converging evidence support investigation of ERK1/2 activity in autism spectrum disorder (ASD). We previously reported enhanced baseline lymphocytic ERK1/2 activation in autism, and now we extend our work to investigate the early phase kinetics of lymphocytic ERK1/2 activation in idiopathic ASD.

Live Cell Microscopy and Flow Cytometry to Study Streptolysin S-Mediated Erythrocyte Hemolysis.

The ability to induce hemolysis, the rupturing of erythrocytes with the consequent release of their intracellular contents, is a phenotypic hallmark of a number of microbial toxins. Streptococcus pyogenes or Group A Streptococcus (GAS) is a human pathogen responsible for a wide range of diseases from mild pharyngitis to severe conditions such as toxic shock syndrome. GAS produces a powerful hemolytic toxin called streptolysin S (SLS).

Effects of Manganese Porphyrins on Cellular Sulfur Metabolism.

Manganese porphyrins (MnPs), MnTE-2-PyP, MnTnHex-2-PyP and MnTnBuOE-2-PyP, are superoxide dismutase (SOD) mimetics and form a redox cycle between O and reductants, including ascorbic acid, ultimately producing hydrogen peroxide (HO). We previously found that MnPs oxidize hydrogen sulfide (HS) to polysulfides (PS; HS, n = 2-6) in buffer. Here, we examine the effects of MnPs for 24 h on HS metabolism and PS production in HEK293, A549, HT29 and bone marrow derived stem cells (BMDSC) using HS (AzMC, MeRho-AZ) and PS (SSP4) fluorophores.

Extended hypoxia-mediated H S production provides for long-term oxygen sensing.

Aim: Numerous studies have shown that H S serves as an acute oxygen sensor in a variety of cells. We hypothesize that H S also serves in extended oxygen sensing.

Methods: Here, we compare the effects of extended exposure (24-48 hours) to varying O tensions on H S and polysulphide metabolism in human embryonic kidney (HEK 293), human adenocarcinomic alveolar basal epithelial (A549), human colon cancer (HTC116), bovine pulmonary artery smooth muscle, human umbilical-derived mesenchymal stromal (stem) cells and porcine tracheal epithelium (PTE) using sulphur-specific fluorophores and fluorometry or confocal microscopy.

Iron Deficiency Reduces Synapse Formation in the Drosophila Clock Circuit.

Iron serves as a critical cofactor for proteins involved in a host of biological processes. In most animals, dietary iron is absorbed in enterocytes and then disseminated for use in other tissues in the body. The brain is particularly dependent on iron.

A Randomized Placebo-Controlled Cross-Over Pilot Study of Riluzole for Drug-Refractory Irritability in Autism Spectrum Disorder.

Riluzole is a glutamatergic modulator of particular interest in autism spectrum disorder (ASD). In this 12-week randomized, double-blind, placebo-controlled, crossover pilot study we evaluated the safety and tolerability of 5-week of adjunctive riluzole treatment (vs. 5-week of placebo, with 2-week washout period) targeting ASD-associated drug-refractory irritability in eight individuals age 12-25 years.

Acamprosate rescues neuronal defects in the Drosophila model of Fragile X Syndrome.

Aims: Several off-label studies have shown that acamprosate can provide some clinical benefits in youth with Fragile X Syndrome (FXS), an autism spectrum disorder caused by loss of function of the highly conserved FMR1 gene. This study investigated the ability of acamprosate to rescue cellular, molecular and behavioral defects in the Drosophila model of FXS.

Main Methods: A high (100μM) and low (10μM) dose of acamprosate was fed to Drosophila FXS (dfmr1 null) or genetic control (w) larvae and then analyzed in multiple paradigms.

Taste Preference Assay for Adult Drosophila.

Olfactory and gustatory perception of the environment is vital for animal survival. The most obvious application of these chemosenses is to be able to distinguish good food sources from potentially dangerous food sources. Gustation requires physical contact with a chemical compound which is able to signal through taste receptors that are expressed on the surface of neurons.

Activation of band 3 mediates group A Streptococcus streptolysin S-based beta-haemolysis.

Streptococcus pyogenes, or group A Streptococcus (GAS), is a human bacterial pathogen that can manifest as a range of diseases from pharyngitis and impetigo to severe outcomes such as necrotizing fasciitis and toxic shock syndrome. GAS disease remains a global health burden with cases estimated at over 700 million annually and over half a million deaths due to severe infections(1). For over 100 years, a clinical hallmark of diagnosis has been the appearance of complete (beta) haemolysis when grown in the presence of blood.

Drosophila Cbp53E Regulates Axon Growth at the Neuromuscular Junction.

Calcium is a primary second messenger in all cells that functions in processes ranging from cellular proliferation to synaptic transmission. Proper regulation of calcium is achieved through numerous mechanisms involving channels, sensors, and buffers notably containing one or more EF-hand calcium binding domains. The Drosophila genome encodes only a single 6 EF-hand domain containing protein, Cbp53E, which is likely the prototypic member of a small family of related mammalian proteins that act as calcium buffers and calcium sensors.

Host Cell Plasma Membrane Phosphatidylserine Regulates the Assembly and Budding of Ebola Virus.

Unlabelled: Lipid-enveloped viruses replicate and bud from the host cell where they acquire their lipid coat. Ebola virus, which buds from the plasma membrane of the host cell, causes viral hemorrhagic fever and has a high fatality rate. To date, little has been known about how budding and egress of Ebola virus are mediated at the plasma membrane.

Molecular and genetic analysis of the Drosophila model of fragile X syndrome.

The Drosophila genome contains most genes known to be involved in heritable disease. The extraordinary genetic malleability of Drosophila, coupled to sophisticated imaging, electrophysiology, and behavioral paradigms, has paved the way for insightful mechanistic studies on the causes of developmental and neurological disease as well as many possible interventions. Here, we focus on one of the most advanced examples of Drosophila genetic disease modeling, the Drosophila model of Fragile X Syndrome, which for the past decade has provided key advances into the molecular, cellular, and behavioral defects underlying this devastating disorder.

Comparative genomic analysis of Drosophila melanogaster and vector mosquito developmental genes.

Genome sequencing projects have presented the opportunity for analysis of developmental genes in three vector mosquito species: Aedes aegypti, Culex quinquefasciatus, and Anopheles gambiae. A comparative genomic analysis of developmental genes in Drosophila melanogaster and these three important vectors of human disease was performed in this investigation. While the study was comprehensive, special emphasis centered on genes that 1) are components of developmental signaling pathways, 2) regulate fundamental developmental processes, 3) are critical for the development of tissues of vector importance, 4) function in developmental processes known to have diverged within insects, and 5) encode microRNAs (miRNAs) that regulate developmental transcripts in Drosophila.

The fragile X mental retardation protein developmentally regulates the strength and fidelity of calcium signaling in Drosophila mushroom body neurons.

Fragile X syndrome (FXS) is a broad-spectrum neurological disorder characterized by hypersensitivity to sensory stimuli, hyperactivity and severe cognitive impairment. FXS is caused by loss of the fragile X mental retardation 1 (FMR1) gene, whose FMRP product regulates mRNA translation downstream of synaptic activity to modulate changes in synaptic architecture, function and plasticity. Null Drosophila FMR1 (dfmr1) mutants exhibit reduced learning and loss of protein synthesis-dependent memory consolidation, which is dependent on the brain mushroom body (MB) learning and memory center.

Fragile X mental retardation protein has a unique, evolutionarily conserved neuronal function not shared with FXR1P or FXR2P.

Fragile X syndrome (FXS), resulting solely from the loss of function of the human fragile X mental retardation 1 (hFMR1) gene, is the most common heritable cause of mental retardation and autism disorders, with syndromic defects also in non-neuronal tissues. In addition, the human genome encodes two closely related hFMR1 paralogs: hFXR1 and hFXR2. The Drosophila genome, by contrast, encodes a single dFMR1 gene with close sequence homology to all three human genes.

Activity-dependent modulation of neural circuit synaptic connectivity.

In many nervous systems, the establishment of neural circuits is known to proceed via a two-stage process; (1) early, activity-independent wiring to produce a rough map characterized by excessive synaptic connections, and (2) subsequent, use-dependent pruning to eliminate inappropriate connections and reinforce maintained synapses. In invertebrates, however, evidence of the activity-dependent phase of synaptic refinement has been elusive, and the dogma has long been that invertebrate circuits are "hard-wired" in a purely activity-independent manner. This conclusion has been challenged recently through the use of new transgenic tools employed in the powerful Drosophila system, which have allowed unprecedented temporal control and single neuron imaging resolution.

Drosophila fragile X mental retardation protein developmentally regulates activity-dependent axon pruning.

Fragile X Syndrome (FraX) is a broad-spectrum neurological disorder with symptoms ranging from hyperexcitability to mental retardation and autism. Loss of the fragile X mental retardation 1 (fmr1) gene product, the mRNA-binding translational regulator FMRP, causes structural over-elaboration of dendritic and axonal processes, as well as functional alterations in synaptic plasticity at maturity. It is unclear, however, whether FraX is primarily a disease of development, a disease of plasticity or both: a distinction that is vital for engineering intervention strategies.

Mammary tumor induction in transgenic mice expressing an RNA-binding protein.

We have analyzed mammary tumors arising in transgenic mice expressing a novel, multifunctional RNA-binding protein. The protein, which we call the c-myc mRNA coding region instability determinant binding protein (CRD-BP), binds to c-myc, insulin-like growth factor II, and beta-actin mRNAs, and to H19 RNA. Depending on the RNA substrate, the CRD-BP affects RNA localization, translation, or stability.