Effect of Activation of the GLT-1 Transporter by a Beta-Lactam Antibiotic on Serotonin-Induced Scratching Behavior in Mice

Glutamate is believed to be the predominant excitatory neurotransmitter in the networks responsible for itch-related behavior. Beta-lactam antibiotics were shown to exert neuroprotective effects by increasing expression of the glutamate transporter GLT-1. We observed whether repeated administration of the beta-lactam antibiotic ceftriaxone suppresses serotonin-induced itch-related behavior (similarly to its effect on pain transmission) in mice. Chronic, but not acute, ceftriaxone introductions reduced the number of serotonin-induced scratches; dihydrokainic acid, a selective GLT-1 transporter inhibitor, partly but significantly abolished this effect of ceftriaxone. Our findings suggest that GLT-1 activation by beta-lactam antibiotics looks promising for the treatment of chronic itch.Як вважають, глутамат є основним збуджуючим нейротрансмітером у нейронних мережах, відповідальних за поведінкові моторні прояви при почутті свербіжу. β-лактамні антибіотики мають нейропротективні властивості, оскільки забезпечують посилену експресію глутаматного транспортера GLT-1. Ми з’ясовували, чи здатне повторне введення β-лактамного антибіотика цефтриаксону пригнічувати викликані ін’єкціями серотоніну поведінкові моторні прояви (чухальні рухи), пов’язані з індукцією почуття свербіжу (подібно до впливу цього агента на біль) у мишей. Хронічні (але не поодинокі) введення цефтриаксону викликали зменшення кількості рухів чухання. Селективний блокатор транспортера GLT-1 дигідрокаїнова кислота частково, але істотно перешкоджала цьому ефекту цефтриаксону. Наші спостереження дають підстави вважати, що активація GLT-1 β-лактамними антибіотиками є перспективним підходом у лікуванні хронічного свербіжу

Characterization and life cycle assessment of geopolymer mortars with masonry units and recycled concrete aggregates assorted from construction and demolition waste

YesDeveloping a fast, cost-effective, eco-friendly solution to recycle large amounts of construction and demolition waste (CDW) generated from construction industry-related activities and natural disasters is crucial. The present investigation aims to offer a solution for repurposing CDW into building materials suitable for accelerated construction and housing in developing countries and disaster-prone areas. Feasibility of recycled concrete aggregate (RCA) inclusion in geopolymer mortars constituted entirely from CDW (masonry elements) was investigated via an environmental impact-oriented approach by addressing the composition related key parameters. Mechanical performance was evaluated through compressive strength tests, and scanning electron microscope (SEM) imaging with line mapping analyses were carried out to monitor the interfacial transition zone (ITZ) properties. To investigate the environmental impacts of the geopolymer mortars and highlight the advantages over Portland cement-based mortars, a cradle-to-gate life cycle assessment (LCA) was performed. Findings revealed that roof tile (RT)-based geopolymer mortars mainly exhibited better strength performance due to their finer particle size. Mixtures activated with 15 M NaOH solution and cured at 105 °C achieved an average compressive strength above 55 MPa. RCA size was the most influential parameter on compressive strength, and a smaller maximum RCA size significantly increased the compressive strength. Microstructural analyses showed that the ITZ around smaller RCAs was relatively thinner, resulting in better compressive strength results. LCA proved that CDW-based geopolymer mortars provide the same compressive strength with around 60% less CO2 emissions and similar energy consumption compared to Portland cement-based mortars.This project has received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement No 894100. The authors also wish to acknowledge the support of the Scientific and Technical Research Council of Turkey (TUBITAK) provided under project: 117M44

Compound 48/80, a histamine-depleting agent, blocks the protective effect of morphine against electroconvulsive shock in mice

We have shown that morphine has an anticonvulsive effect against maximal electroconvulsive shock (MES) in mice, and this effect is antagonized by histamine H1-receptor antagonists. Brain histamine is localized both in neurons and in mast cells, and morphine is known to enhance the turnover of neuronal histamine and to release histamine from mast cells. In the present experiments, compound 48/80 was injected chronically (0.5 mg/kg on day 1, 1 mg/kg on day 2, 2 mg/kg on day 3, 3 mg/kg on day 4, and 4 mg/kg on day 5, twice daily, ip) to deplete mast cell contents. Morphine (0.001-10 mg/kg, ip; N = 20) produced a dose-dependent anticonvulsive effect against MES seizure in mice with non-depleted mast cells, whereas it did not exert any anticonvulsive effect in mice with depleted mast cells. These results indicate that morphine produces its anticonvulsive effect against maximal electroconvulsive shock in mice by liberating histamine from mast cells