Effects and safety of on depression: a systematic review and meta-analysis.

Because depression is a major factor contributing to the global disease burden, we tried to analyze the effects and safety of (GKB) on patients with depression. We conducted a literature search for articles published between January 2002 and May 2022 in seven online databases (PubMed, Scopus, Embase, Google Scholar, Web of Sciences, Cochrane Library, and China National Knowledge Infrastructure). A systematic literature review and meta-analysis were performed to compare the effects and safety of GKB on patients with depression, including subjective and objective indicators of depression evaluation.

Atypical and delayed spinal cord MRI features of COVID-19-associated myelopathies: a report of four cases and literature review.

We reported four patients with coronavirus disease 2019 (COVID-19)-associated myelopathies, highlighting the delayed and atypical spinal cord magnetic resonance imaging (MRI) features and the literature review. All four patients were males, aged 37 to 72 years old. The latencies from COVID-19 to the onset of myelitis were 5, 15, 30, and 80 days.

Effects of tau on Aβ-induced synaptic damage in a Drosophila model of Alzheimer's disease.

Objectives: The etiology and pathologic mechanism underlying Alzheimer's disease (AD) are not clear. This study determined the effects of tau on amyloid-beta peptide(Aβ)-induced synaptic damages in a Drosophila model of AD.

Methods: Galactose-regulated upstream promoter element 4(Gal4) and an upstream active sequence system was used to establish four kinds of Aβ transgenic Drosophila models of AD.

Plant AFC2 kinase desensitizes thermomorphogenesis through modulation of alternative splicing.

High ambient temperatures have adverse impacts on crop yields. Although a few plant thermosensors have been reported, these sensors directly or indirectly impact PIF4-controlled transcriptional regulation. Moreover, high temperatures also trigger a number of post-transcriptional alternative splicing events in plants and even in animals.

MoS Decorated Silver Nanowire-Reduced Graphene Oxide Aerogel Micro-Particle for Thermally Conductive Polymer Composites with Enhanced Flame Retardancy.

Multifunctional polymer composites with efficient heat dissipation and flame retardancy are highly desirable in the electronic industry. Here, by the combination of hydrothermal reaction and in situ fragmentation, molybdenum disulfide (MoS ) decorated silver nanowires (AgNWs) and 3D reduced graphene oxide (RGO) (AgNW-RGO@MoS ) aerogel micro-particles (AMPs) are successfully prepared. When the above AMP is introduced to epoxy (EP) resin by the simple blending method, a polymer composite with continuous thermally conductive pathways and flame barrier layers is achieved.

Plant responses to high temperature: a view from pre-mRNA alternative splicing.

This review focused on the recent breakthroughs in plant high temperature responses from an alternative splicing angle. With the inevitable global warming, high temperature triggers plants to change their growth and developmental programs for adapting temperature increase. In the past decades, the signaling mechanisms from plant thermo-sensing to downstream transcriptional cascades have been extensively studied.

PIF4 and HOOKLESS1 Impinge on Common Transcriptome and Isoform Regulation in Thermomorphogenesis.

High temperature activates the transcription factor PHYTOCHROME-INTERACTING FACTOR4 (PIF4) to stimulate auxin signaling, which causes hypocotyl elongation and leaf hyponasty (thermomorphogenesis). HOOKLESS1 (HLS1) is a recently reported positive regulator of thermomorphogenesis, but the molecular mechanisms by which HLS1 regulates thermomorphogenesis remain unknown. In this study, we initially compared PIF4- and/or HLS1-dependent differential gene expression (DEG) upon high-temperature treatment.

Emerging Plant Thermosensors: From RNA to Protein.

How plants sense temperature is an important question. Here, we highlight recent achievements in identifying plant thermosensors, including RNA switch and protein-DNA binding ability. Finally, we borrow an idea from one recent mammalian study and propose a putative temperature-sensitive kinase as a thermosensory mechanism.

Levodopa/Benserazide PLGA Microsphere Prevents L-Dopa-Induced Dyskinesia Lower β-Arrestin2 in 6-Hydroxydopamine Parkinson's Rats.

Prolonged pulsatile administration of Levodopa (L-dopa) can generate L-dopa-induced dyskinesia (LID). Numerous research has reported that continuous dopamine delivery (CDD) was useful in reducing the severity of LID. 6-OHDA lesioned rats were divided into two groups to receive intermittent L-dopa stimulation (L-dopa/benserazide) or Levodopa/benserazide PLGA microsphere (LBPM) for 3 weeks.

Idebenone Alleviates Neuroinflammation and Modulates Microglial Polarization in LPS-Stimulated BV2 Cells and MPTP-Induced Parkinson's Disease Mice.

Idebenone is an antioxidant and a coenzyme Q10 analog that has been used to treat neurodegeneration disease. Some studies show idebenone exerts anti-inflammatory effects. However, whether idebenone can be used to reduce the neuroinflammation in Parkinson's disease (PD) has been little studied.

Partial Depletion of Peripheral M1 Macrophages Reverses Motor Deficits in MPTP-Treated Mouse by Suppressing Neuroinflammation and Dopaminergic Neurodegeneration.

Neuroinflammation plays an important role in the pathogenesis of Parkinson's disease (PD). Inflammatory cytokines in the peripheral immune system can induce neuroinflammation in central nervous system (CNS). Whether the peripheral immune system is involved in PD is unclear.

Antidyskinetic Treatment with MTEP Affects Multiple Molecular Pathways in the Parkinsonian Striatum.

Parkinson's disease is characterized by dopaminergic neuron loss and dopamine (DA) depletion in the striatum. Standard treatment is still focused on the restoration of dopamine with exogenous L-Dopa, which however causes L-Dopa-induced dyskinesia (LID). Several studies have shown that antagonism of the metabotropic glutamate receptor 5 alleviates LID, but the underlying mechanisms have remained unclear.

Lipoic acid alleviates L‑DOPA‑induced dyskinesia in 6‑OHDA parkinsonian rats via anti‑oxidative stress.

Levodopa (L‑DOPA) is the gold standard for symptomatic treatment of Parkinson's disease (PD); however, long‑term therapy is associated with the emergence of L‑DOPA‑induced dyskinesia (LID). Nigral dopaminergic cell loss determines the degree of drug exposure and time required for the initial onset of LID. Accumulating evidence indicates that α‑lipoic acid (ALA) decreases this nigral dopaminergic cell loss.

Current Experimental Studies of Gene Therapy in Parkinson's Disease.

Parkinson's disease (PD) was characterized by late-onset, progressive dopamine neuron loss and movement disorders. The progresses of PD affected the neural function and integrity. To date, most researches had largely addressed the dopamine replacement therapies, but the appearance of L-dopa-induced dyskinesia hampered the use of the drug.

Inhibition of Glycogen Synthase Kinase-3β (GSK-3β) as potent therapeutic strategy to ameliorates L-dopa-induced dyskinesia in 6-OHDA parkinsonian rats.

Levodopa (L-dopa) is the dominating therapy drug for exogenous dopaminergic substitution and can alleviate most of the manifestations of Parkinson's disease (PD), but long-term therapy is associated with the emergence of L-dopa-induced dyskinesia (LID). Evidence points towards an involvement of Glycogen Synthase Kinase-3β (GSK-3β) in development of LID. In the present study, we found that animals rendered dyskinetic by L-dopa treatment, administration of TDZD8 (2mg/kg) obviously prevented the severity of AIM score, as well as improvement in motor function (P < 0.

Intraneuronal accumulation of Aβ42 induces age-dependent slowing of neuronal transmission in Drosophila.

Beta amyloid (Aβ42)-induced dysfunction and loss of synapses are believed to be major underlying mechanisms for the progressive loss of learning and memory abilities in Alzheimer's disease (AD). The vast majority of investigations on AD-related synaptic impairment focus on synaptic plasticity, especially the decline of long-term potentiation of synaptic transmission caused by extracellular Aβ42. Changes in other aspects of synaptic and neuronal functions are less studied or undiscovered.