Dual-Component Gas Sensor Based on Light-Induced Thermoelastic Spectroscopy and Deep Learning.

In this paper, an acetylene-carbon dioxide dual-component gas sensor based on light-induced thermoelastic spectroscopy and deep learning is reported for the first time. Two lasers with wavelengths of 1530 and 1577 nm were coupled by a wavelength division multiplexer to excite the two gas molecules. The sensor combined four algorithms, namely, sparrow search algorithm (SSA), convolutional neural network (CNN), bidirectional gated recurrent unit neural network (BiGRU), and attention mechanism (Attention), to achieve two-component gas concentration inversion in three cases, in which the overlap of the two gas spectral lines is different.

Targeted ErbB4 receptor activation prevents D-galactose-induced neuronal senescence via inhibiting ferroptosis pathway.

Background: Neuronal senescence is a common pathological feature of various neurodegenerative diseases, with ferroptosis playing a significant role. This study aims to investigate the role of ErbB4 receptor activation in preventing D-Galactose (D-gal)-induced neuronal senescence.

Methods: Mice subjected to D-gal-induced aging were administered a small molecule ErbB4 receptor agonist (E4A), identified via virtual screening, melatonin, or a combination of both.

Indoleamine 2, 3-dioxygenase 1 inhibition mediates the therapeutic effects in Parkinson's disease mice by modulating inflammation and neurogenesis in a gut microbiota dependent manner.

Abnormal tryptophan metabolism is closely linked with neurological disorders. Research has shown that indoleamine 2,3-dioxygenase 1 (IDO-1), the first rate-limiting enzyme in tryptophan degradation, is upregulated in Parkinson's disease (PD). However, the precise role of IDO-1 in PD pathogenesis remains elusive.

Mechanism of S100A9-mediated astrocyte activation via TLR4/NF-κB in Parkinson's disease.

Astrocyte-mediated neuroinflammation plays a key role in Parkinson's disease (PD) progression. The proinflammatory protein S100A9 is linked to various neurodegenerative diseases, but its involvement in astrocyte activation in PD remains unclear. Here, we investigate the role of S100A9 in astrocyte-mediated neuroinflammation in PD.

Molecular subtypes based on immunologic and epithelial-mesenchymal transition gene sets reveal tumor immune microenvironment characteristics and implications for immunotherapy of patients with glioma.

The tumor immune microenvironment (TIME) significantly influences cancer progression and treatment. This study sought to uncover novel TIME-related glioma biomarkers to advance antitumor immunotherapies by integrating data from sequencing of bulk RNA as well as scRNA. Immunologic and epithelial-mesenchymal transition (EMT) characteristics were used to classify glioma patients into two immune subtypes (ISs) and two EMT subtypes (ESs).

A surrogate-assisted extended generative adversarial network for parameter optimization in free-form metasurface design.

Metasurfaces have widespread applications in fifth-generation (5G) microwave communication. Among the metasurface family, free-form metasurfaces excel in achieving intricate spectral responses compared to regular-shape counterparts. However, conventional numerical methods for free-form metasurfaces are time-consuming and demand specialized expertise.

Positive Effect of 6-Gingerol on Functional Plasticity of Microglia in a rat Model of LPS-induced Depression.

Neuroinflammation has emerged as a crucial factor in the development of depression. Despite the well-known anti-inflammatory properties of 6-gingerol, its potential impact on depression remains poorly understood. This study aimed to investigate the antidepressant effects of 6-gingerol by suppressing microglial activation.

A Pilot Study on a Possible Mechanism behind Olfactory Dysfunction in Parkinson's Disease: The Association of TAAR1 Downregulation with Neuronal Loss and Inflammation along Olfactory Pathway.

Parkinson's disease (PD) is characterized not only by motor symptoms but also by non-motor dysfunctions, such as olfactory impairment; the cause is not fully understood. Our study suggests that neuronal loss and inflammation in brain regions along the olfactory pathway, such as the olfactory bulb (OB) and the piriform cortex (PC), may contribute to olfactory dysfunction in PD mice, which might be related to the downregulation of the trace amine-associated receptor 1 (TAAR1) in these areas. In the striatum, although only a decrease in mRNA level, but not in protein level, of TAAR1 was detected, bioinformatic analyses substantiated its correlation with PD.

Is Beneficial to a Mouse Model of Parkinson's Disease, via Alleviated Neuroinflammation and Promoted Neurogenesis, with Involvement of SCFAs.

Increasing evidence suggests that the gut microbiota may represent potential strategies for Parkinson's disease (PD) treatment. Our previous research revealed a decreased abundance of (Akk) in PD mice; however, whether Akk is beneficial to PD is unknown. To answer this question, the mice received MPTP intraperitoneally to construct a subacute model of PD and were then supplemented with Akk orally for 21 consecutive days.

Neuregulin 4 (Nrg4) cooperates with melatonin to regulate the PRL expression via ErbB4/Erk signaling pathway as a potential prolactin (PRL) regulator.

Neuregulin-4 (Nrg4) and melatonin play vital roles in endocrine diseases. However, there is little discussion about the function and potential mechanism of Nrg4 and melatonin in prolactin (PRL) regulation. The human normal pituitary data from Gene Expression Profiling Interactive Analysis (GEPIA) database was used to explore the correlation between NRG4 and PRL.

Reducing polypyrimidine tract‑binding protein 1 fails to promote neuronal transdifferentiation on HT22 and mouse astrocyte cells under physiological conditions.

In contrast to prior findings that have illustrated the conversion of non-neuronal cells into functional neurons through the specific targeting of polypyrimidine tract-binding protein 1 (PTBP1), accumulated evidence suggests the impracticality of inducing neuronal transdifferentiation through suppressing PTBP1 expression in pathological circumstances. Therefore, the present study explored the effect of knocking down PTBP1 under physiological conditions on the transdifferentiation of mouse hippocampal neuron HT22 cells and mouse astrocyte (MA) cells. A total of 20 µM negative control small interfering (si)RNA and siRNA targeting PTBP1 were transfected into HT22 and MA cells using Lipo8000 for 3 and 5 days, respectively.

5-HT4 Receptor is Protective for MPTP-induced Parkinson's Disease Mice Via Altering Gastrointestinal Motility or Gut Microbiota.

Serotonergic dysfunction is related to both motor and nonmotor symptoms in Parkinson's disease (PD). As a 5-HT receptor, 5-HT4 receptor (5-HT4R) is well-studied and already-used in clinical therapy of constipation, which is a typical non-motor symptom in PD. In this study, we investigated the role of 5-HT4R as a regulator of gut function in MPTP-induced acute PD mice model.

Research on ferroptosis as a therapeutic target for the treatment of neurodegenerative diseases.

Ferroptosis is an iron- and lipid peroxidation (LPO)-mediated programmed cell death type. Recently, mounting evidence has indicated the involvement of ferroptosis in neurodegenerative diseases, especially in Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), Huntington's disease (HD), and so on. Treating ferroptosis presents opportunities as well as challenges for neurodegenerative diseases.

Fecal Microbiota Transplantation from Aged Mice Render Recipient Mice Resistant to MPTP-Induced Nigrostriatal Degeneration Via a Neurogenesis-Dependent but Inflammation-Independent Manner.

Accumulating data support a crucial role of gut microbiota in Parkinson's disease (PD). However, gut microbiota vary with age and, thus, will affect PD in an age-dependent, but unknown manner. We examined the effects of fecal microbiota transplantation (FMT) pretreatment, using fecal microbiota from young (7 weeks) or aged mice (23 months), on MPTP-induced PD model.

Multifunctional High Entropy Alloys Enabled by Severe Lattice Distortion.

Since 2004, the design of high entropy alloys (HEAs) has generated significant interest within the materials science community due to their exceptional structural and functional properties. By incorporating multiple principal elements into a common lattice, it is possible to create a single-phase crystal with a highly distorted lattice. This unique feature enables HEAs to offer a promising combination of mechanical and physical properties that are not typically observed in conventional alloys.

Involvement of CXCL10 in Neuronal Damage under the Condition of Spinal Cord Injury and the Potential Therapeutic Effect of Nrg1.

Objective: Few studies have reported the direct effect of C-X-C motif chemokine ligand 10 (CXCL10) and Neuregulin 1 (Nrg1) on neurons after spinal cord injury (SCI). This study reports the role of CXCL10 in the regulation of neuronal damage after SCI and the potential therapeutic effect of Nrg1.

Methods: The expression level of and in SCI mice was analyzed in the Gene Expression Omnibus DataSets, followed by immunohistochemical confirmation using a mouse SCI model.

Age-related decline in hippocampal tyrosine phosphatase PTPRO is a mechanistic factor in chemotherapy-related cognitive impairment.

Chemotherapy-related cognitive impairment (CRCI) or "chemo brain" is a devastating neurotoxic sequela of cancer-related treatments, especially for the elderly individuals. Here we show that PTPRO, a tyrosine phosphatase, is highly enriched in the hippocampus, and its level is tightly associated with neurocognitive function but declined significantly during aging. To understand the protective role of PTPRO in CRCI, a mouse model was generated by treating Ptpro-/- female mice with doxorubicin (DOX) because Ptpro-/- female mice are more vulnerable to DOX, showing cognitive impairments and neurodegeneration.

A prognostic biomarker NRG1 promotes U-87 MG glioblastoma cell malignancy by inhibiting autophagy via ERBB2/AKT/mTOR pathway.

Glioblastoma (GBM) is the most common and aggressive primary brain malignancy. Studies have shown that autophagy-related (ATG) genes play important roles in regulating GBM malignancy. However, the mechanism still needs to be fully elucidated.

Orally Induced High Serum Level of Trimethylamine N-oxide Worsened Glial Reaction and Neuroinflammation on MPTP-Induced Acute Parkinson's Disease Model Mice.

Neuroinflammation mediated by brain glial cells is one of the pathological drivers of Parkinson's disease (PD). Recent studies have shown that higher circulating trimethylamine N-oxide (TMAO, a gut microbiota-derived metabolite) can induce neuroinflammation and are strongly related to a variety of central nervous system diseases and adverse brain events. Herein, we explored the effect of pre-existing higher circulating TMAO on dopamine system and neuroinflammation in acute PD model mice induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydroxypyridine (MPTP).

Trimethylamine N-Oxide Exacerbates Neuroinflammation and Motor Dysfunction in an Acute MPTP Mice Model of Parkinson's Disease.

Observational studies have shown abnormal changes in trimethylamine N-oxide (TMAO) levels in the peripheral circulatory system of Parkinson's disease (PD) patients. TMAO is a gut microbiota metabolite that can cross the blood-brain barrier and is strongly related to neuroinflammation. Neuroinflammation is one of the pathological drivers of PD.

Current study on diagnosis and treatment of Alzheimer's disease by targeting amyloid b-protein.

Alzheimer's disease (AD), also known as senile dementia, is a degenerative disease of the central nervous system and is characterized by insidious onset and a chronic progressive course. It is the most common type of senile dementia. Studies have proved that the deposition of amyloid b (Ab) in the brain is one of the initiating factors correlated to the pathology of AD, and it acts as one of the critical factors leading to the onset of AD.

Nuclear translocation of cGAS orchestrates VEGF-A-mediated angiogenesis.

Cyclic GMP-AMP synthase (cGAS) senses cytosolic incoming DNA and consequently activates stimulator of interferon response cGAMP interactor 1 (STING) to mount immune response. Here, we show nuclear cGAS could regulate VEGF-A-mediated angiogenesis in an immune-independent manner. We found VEGF-A stimulation induces cGAS nuclear translocation via importin-β pathway.