Supplier-origin gut microbiomes affect host body weight and select autism-related behaviors.

Autism spectrum disorders (ASD) are complex human neurodiversities increasing in prevalence within the human population. In search of therapeutics to improve quality-of-life for ASD patients, the gut microbiome (GM) has become a promising target as a growing body of work supports roles for the complex community of microorganisms in influencing host behavior via the gut-brain-axis. However, whether naturally-occurring microbial diversity within the host GM affects these behaviors is often overlooked.

Producing Blends of Polybutylene Adipate Terephthalate and Blood Meal That Are Safe to Render.

Single-use plastic hygiene control products used during red meat processing can have severe negative impacts on the environment and cannot be processed with offal during rendering into meat and bone meal. However, plastics made from protein could potentially solve this problem as the material would be safe to render. The objective of this work was to prepare blends of blood meal and polybutylene adipate terephthalate (PBAT) in the absence of water using the interaction between PBAT and protein as the plasticisation mechanism.

Filamentous fungi for future functional food and feed.

In this review, we offer our opinion of current and expected trends regarding the use of mushrooms and mycelia in food and feed. Mushrooms have provided food for millennia and production methods and species diversity have recently expanded. Beyond mushrooms, cultured fungal mycelia are now harvested as a primary product for food.

Development of simple, scalable protease production from Botrytis cinerea.

Heat haze-forming proteins are stable during winemaking and are typically removed via adsorption to bentonite. Proteolytic degradation is an alternative method to prevent wine-haze and offers the opportunity to reduce the environmental impacts and labor cost of the process. Herein, we describe the development of a production system for Botrytis cinerea proteases for the enzymatic degradation of heat haze-forming proteins.

Novel sequence types of Chlamydia pecorum infect free-ranging Alpine ibex (Capra ibex) and red deer (Cervus elaphus) in Switzerland.

Chlamydia pecorum, a recognized pathogen of domesticated ruminants and koalas (Phascolarctos cinereus), has been recently reported in a broad range of other wildlife species including water buffalo (Bubalus bubalis), ibex (Capra ibex), chamois (Rupicapra rupicapra), red deer (Cervus elaphus), and birds. This identification raises questions as to whether cross-host transmission may be a factor in the epidemiology of infections in these species. To begin to address this question, we employed a C.

Neurodegenerative effects of recombinant HIV-1 Tat(1-86) are associated with inhibition of microtubule formation and oxidative stress-related reductions in microtubule-associated protein-2(a,b).

The human immunodeficiency virus 1 (HIV-1) protein Trans-activator of Transcription (Tat) is a nuclear regulatory protein that may contribute to the development of HIV-1 associated dementia by disrupting the neuronal cytoskeleton. The present studies examined effects of recombinant Tat(1-86; 1-100 nM) on microtubule-associated protein (MAP)-dependent and MAP-independent microtubule formation ex vivo and oxidative neuronal injury in rat organotypic hippocampal explants. Acute exposure to Tat(1-86) (≥1 nM) markedly reduced MAP-dependent and -independent microtubule formation ex vivo, as did vincristine sulfate (0.

Exercise for depression: efficacy, safety and clinical trial implications.

Exercise is gaining interest as a treatment for major depressive disorder (MDD). Though not yet fully established as an efficacious therapy for psychiatric disorders, exercise has well-established benefits for physical health and overall well-being. However, there are potential health risks to exercise that need to be considered before recommending physical activity to a patient.

Sex differences in the neurotoxic effects of adenosine A1 receptor antagonism during ethanol withdrawal: reversal with an A1 receptor agonist or an NMDA receptor antagonist.

Background: Neuronal adaptations that occur during chronic ethanol (EtOH) exposure have been observed to sensitize the brain to excitotoxic insult during withdrawal. The adenosine receptor system warrants further examination in this regard, as recent evidence has implicated adenosine receptor involvement in the behavioral effects of both EtOH exposure and withdrawal.

Methods: The current studies examined effects of adenosine A(1) receptor manipulation on neuronal injury in EtOH-naive and EtOH-withdrawn male and female rat hippocampal slice cultures.

Potentiation of N-methyl-D-aspartate receptor-mediated neuronal injury during methamphetamine withdrawal in vitro requires co-activation of IP3 receptors.

Recent findings suggest that methamphetamine (METH) functions acutely to inhibit N-methyl-d-aspartate (NMDA) receptor function. Protracted withdrawal from METH exposure may increase the sensitivity of NMDA receptors to agonist exposure, promoting neuronal excitability. However, the relevance of METH effects on NMDA receptor activity with regard to neuronal viability has not been fully studied.

Methamphetamine exposure antagonizes N-methyl-D-aspartate receptor-mediated neurotoxicity in organotypic hippocampal slice cultures.

Glutamatergic systems have been increasingly recognized as mediators of methamphetamine's (METH) pharmacological effects though little is known about the means by which METH interacts with glutamate receptors. The present studies examined effects of METH (0.1-100 microM) on [3H]MK-801 binding to membranes prepared from adult rat cortex, hippocampus and cerebellum, as well as the neurotoxicity produced by 24-h exposure to N-methyl-D-aspartate (5-10 microM; NMDA) employing organotypic hippocampal slice cultures of neonatal rat.

A 24 h corticosterone exposure exacerbates excitotoxic insult in rat hippocampal slice cultures independently of glucocorticoid receptor activation or protein synthesis.

Elevations in circulating concentrations of glucocorticoids (GC) may increase the expression and/or sensitivity of ionotropic transmitter receptors in brain. For example, recent evidence suggests that acute and chronic GC exposure may alter the number and/or function of N-methyl-D-aspartate (NMDA)-type glutamate receptors, effects that may sensitize the brain to excitotoxic insults. The present studies examined the ability of short-term (24 h) corticosterone (CORT) exposure to potentiate NMDA-induced cytotoxicity in rat hippocampal slice cultures.

Ethanol exposure and withdrawal sensitizes the rat hippocampal CA1 pyramidal cell region to beta-amyloid (25-35)-induced cytotoxicity: NMDA receptor involvement.

Background: Millions of Americans suffer from Alzheimer's Disease (AD), which is characterized by significant neurological impairment and an accumulation in brain tissue of senile plaques consisting of beta amyloid (Abeta) peptide. The hippocampus, a region primarily responsible for learning and memory, appears to be particularly susceptible to AD-related injury and chronic alcohol abuse. Although certain risk factors for AD are known, it is unclear if alcohol abuse or dependence may contribute to neuropathology in AD.

Corticosterone increases damage and cytosolic calcium accumulation associated with ethanol withdrawal in rat hippocampal slice cultures.

Background: Evidence suggests that stress hormones (i.e., glucocorticoids) may be increased during acute or chronic consumption of ethanol and during withdrawal from ethanol consumption, effects that may contribute to the development of cognitive impairment.

Cytotoxic effects of exposure to the human immunodeficiency virus type 1 protein Tat in the hippocampus are enhanced by prior ethanol treatment.

Background: Long-term ethanol exposure leads to increases in the expression and/or sensitivity of NMDA-type glutamate receptors, effects that may contribute to the development of cytotoxicity in the brain. The human immunodeficiency virus 1 (HIV-1) transcription factor Tat is one of many viral proteins that may contribute to the development of HIV-associated dementia (HAD) by indirectly or directly promoting excess function of NMDA receptors. Thus, these studies examined the hypothesis that long-term ethanol pre-exposure would sensitize the hippocampus to Tat-induced cytotoxicity in an NMDA receptor-dependent manner.

Choline exposure reduces potentiation of N-methyl-D-aspartate toxicity by corticosterone in the developing hippocampus.

Exposure to high levels of glucocorticoids (GCs) may adversely affect neuronal viability, particularly in the developing hippocampus, via increased function or sensitivity of N-methyl-D-aspartate (NMDA)-type glutamate receptors. Conversely, choline supplementation in the developing brain may reduce the severity of subsequent insult. The present studies aimed to examine the extent to which short-term exposure to high concentrations of corticosterone would produce neuronal injury mediated by NMDA receptor activity.

The human immunodeficiency virus type-1 transcription factor Tat produces elevations in intracellular Ca2+ that require function of an N-methyl-D-aspartate receptor polyamine-sensitive site.

Human immunodeficiency virus type-1 (HIV-1) infection is commonly associated with neuronal loss, as well as, cognitive and motor deficits collectively termed HIV-1-associated dementia (HAD). Function of the HIV-1 transcription factor Tat, activation of N-methyl-D-aspartate (NMDA)-type glutamate receptors, and subsequent rapid rises in free intracellular Ca2+ have been implicated in the development of this neurological disorder. However, the role of specific NMDA receptor modulatory sites in mediating effects of Tat has not been examined.

Opposing effects of ethanol and nicotine on hippocampal calbindin-D28k expression.

Long-term ethanol exposure produces multiple neuroadaptations that likely contribute to dysregulation of Ca(2+) balance and neurotoxicity during ethanol withdrawal. Conversely, nicotine exposure may reduce the neurotoxic consequences of Ca(2+) dysregulation, putatively through up-regulation of the Ca(2+)-buffering protein calbindin-D(28k). The current studies were designed to examine the extent to which 10-day ethanol exposure and withdrawal altered calbindin-D(28k) expression in rat hippocampus.

Neurotoxic effects of the human immunodeficiency virus type-1 transcription factor Tat require function of a polyamine sensitive-site on the N-methyl-D-aspartate receptor.

Human immunodeficiency virus type-I (HIV-1) infection is often associated with neuronal loss in cortical and subcortical regions that may manifest as motor dysfunction and dementia. The function of the HIV-1 transcription protein Tat and subsequent activation of N-methyl-D-aspartate receptors (NMDAr) have been implicated in this form of neurodegeneration. However, it is unclear if Tat interacts directly with the NMDAr and the role of specific NMDAr subunit composition in mediating effects of Tat is also unclear.