Fecal microbiota transplantation alleviates neuronal Apoptosis, necroptosis and reactive microglia activation after ischemic stroke.

Objective: This study aims to delve into the mechanisms underlying the improvement of neurological function in rats with ischemic stroke through fecal microbiota transplantation.

Methods: A total of fifty male Sprague-Dawley rats were categorized into four groups: Sham, MCAO, MCAO+vehicle and FMT. We assessed behavioral and pathological alterations in the rats using modified neurological function scoring and TTC staining.

Phenome-wide association study in 25,639 pregnant Chinese women reveals loci associated with maternal comorbidities and child health.

Phenome-wide association studies (PheWAS) have been less focused on maternal diseases and maternal-newborn comorbidities, especially in the Chinese population. To enhance our understanding of the genetic basis of these related diseases, we conducted a PheWAS on 25,639 pregnant women and 14,151 newborns in the Chinese Han population using ultra-low-coverage whole-genome sequence (ulcWGS). We identified 2,883 maternal trait-associated SNPs associated with 26 phenotypes, among which 99.

Single-nucleus analysis reveals microenvironment-specific neuron and glial cell enrichment in Alzheimer's disease.

Background: Alzheimer's disease (AD) is a complicated neurodegenerative disease. Neuron-glial cell interactions are an important but not fully understood process in the progression of AD. We used bioinformatic methods to analyze single-nucleus RNA sequencing (snRNA-seq) data to investigate the cellular and molecular biological processes of AD.

Asparagine endopeptidase deficiency mitigates radiation-induced brain injury by suppressing microglia-mediated neuronal senescence.

Mounting evidence supports the role of neuroinflammation in radiation-induced brain injury (RIBI), a chronic disease characterized by delayed and progressive neurological impairment. Asparagine endopeptidase (AEP), also known as legumain (LGMN), participates in multiple malignancies and neurodegenerative diseases and may potentially be involved in RIBI. Here, we found AEP expression was substantially elevated in the cortex and hippocampus of wild-type () mice following whole-brain irradiation.

Single-cell and spatial transcriptomics reveals that PTPRG activates the mA methyltransferase VIRMA to block mitophagy-mediated neuronal death in Alzheimer's disease.

Neuronal death is one of the key pathologies in Alzheimer's disease (AD). How neuronal death begins in AD is far from clear, so clarifying this process may help develop effective therapies. This study collected single-cell RNA sequencing data of 85 AD samples and 83 control samples, covering the prefrontal cortex, internal olfactory cortex, superior parietal lobe, superior frontal gyrus, caudal internal olfactory cortex, somatosensory cortex, hippocampus, superior frontal cortex and peripheral blood mononuclear cells.

Development of a low-cost and accurate carrier screening method for spinal muscular atrophy in developing countries.

Heterozygous carriers of the survival of motor neuron 1 (SMN1) gene deletion in parents account for approximately 95% of neonatal spinal muscular atrophy cases. Given the severity of the disease, professional organizations have recommended periconceptional spinal muscular atrophy carrier screening to all couples, regardless of race or ethnicity. However, the prevalence of screening activities in mainland China remains suboptimal, mainly attributed to the limitations of the existing carrier screening methods.

Exploration of novel biomarkers in Alzheimer's disease based on four diagnostic models.

Background: Despite tremendous progress in diagnosis and prediction of Alzheimer's disease (AD), the absence of treatments implies the need for further research. In this study, we screened AD biomarkers by comparing expression profiles of AD and control tissue samples and used various models to identify potential biomarkers. We further explored immune cells associated with these biomarkers that are involved in the brain microenvironment.

Potential biomarkers of Alzheimer's disease and cerebral small vessel disease.

Background: Cerebral small vessel disease (CSVD) is associated with the pathogenesis of Alzheimer's disease (AD). Effective treatments to alleviate AD are still not currently available. Hence, we explored markers and underlying molecular mechanisms associated with AD by utilizing gene expression profiles of AD and CSVD patients from public databases, providing more options for early diagnosis and its treatment.

Identification of molecular signatures associated with sleep disorder and Alzheimer's disease.

Background: Alzheimer's disease (AD) and sleep disorders are both neurodegenerative conditions characterized by impaired or absent sleep. However, potential common pathogenetic mechanisms of these diseases are not well characterized.

Methods: Differentially expressed genes (DEGs) were identified using publicly available human gene expression profiles GSE5281 for AD and GSE40562 for sleep disorder.

REPS1 as a Potential Biomarker in Alzheimer's Disease and Vascular Dementia.

Vascular dementia (VD) and Alzheimer's disease (AD) are common types of dementia for which no curative therapies are known. In this study, we identified hub genes associated with AD and VD in order to explore new potential therapeutic targets. Genes differentially expressed in VD and AD in all three datasets (GSE122063, GSE132903, and GSE5281) were identified and used to construct a protein-protein interaction network.

Primary Coenzyme Q10 Deficiency-7 and Pathogenic Variants: Clinical Presentation, Biochemical Analyses, and Treatment.

Primary Coenzyme Q10 Deficiency-7 (COQ10D7) is a rare mitochondrial disorder caused by pathogenic variants. In this review, we discuss the correlation of genotypes, particularly the East Asian-specific c.370G > A variant, with the clinical presentations and therapeutic effectiveness of coenzyme Q10 supplementation from an exon-dependent perspective.

Bone mesenchymal stromal cells exhibit functional inhibition but no chromosomal aberrations in chronic myelogenous leukemia.

Chronic myelogenous leukemia (CML) is a myeloproliferative neoplasia characterized by the presence of the Philadelphia (Ph) chromosome in hematopoietic cells (HCs). As one of the most important components of the bone marrow microenvironment (BMM), bone mesenchymal stromal cells (BMSCs) are critical in the development of leukemia and essential in the regulation of hematopoiesis. However, little is known regarding the alterations of BMSCs in CML.

Exosomes derived from acute myeloid leukemia cells promote chemoresistance by enhancing glycolysis-mediated vascular remodeling.

Acute myeloid leukemia (AML) is the most common type of leukemia in adults. AML cells secrete angiogenic factors to remodel vasculature and acquire chemoresistance; however, antiangiogenic drugs are often ineffective in AML treatment. Cancer cell-derived exosomes can induce angiogenesis, but their role in vascular remodeling during AML is unclear.

Melatonin inhibits epithelial‑to‑mesenchymal transition in gastric cancer cells via attenuation of IL‑1β/NF‑κB/MMP2/MMP9 signaling.

Although melatonin has been shown to exert marked antitumor effects against a variety of cancers, the underlying mechanisms remain to be fully elucidated. It has been hypothesized that the anticancer properties of melatonin are associated with its ability to suppress epithelial‑to‑mesenchymal transition (EMT) of cancer cells. In the present study, melatonin effectively suppressed interleukin (IL)‑1β‑induced EMT in human gastric adenocarcinoma (GA) cells.

PI3K/Akt inhibitor LY294002 potentiates homoharringtonine antimyeloma activity in myeloma cells adhered to stromal cells and in SCID mouse xenograft.

Homoharringtonine (HHT) is a known anti-leukemia drug that inhibits multiple myeloma (MM) cells both in vitro and in vivo. Our prior study demonstrated that the potency of HHT in MM cells was compromised significantly when myeloma cells were co-cultured with BM stromal cells. This study aimed to investigate whether PI3K/Akt inhibitor LY294002 could potentiate the antimyeloma activity of HHT against MM cells adhered to BM stromal cells and in vivo xenograft models.

Homoharringtonine enhances bortezomib antimyeloma activity in myeloma cells adhesion to bone marrow stromal cells and in SCID mouse xenografts.

Despite the great progress in the treatment, multiple myeloma (MM) still remains incurable. Bortezomib (BTZ), a reversible inhibitor of the 26S proteasome, is very effective against MM but unable to eradicate the MM cells in bone marrow niche eventually causing the disease relapse. Homoharringtonine (HHT) is a known anti-leukemia drug that inhibits MM both in vitro and in vivo.

[Effect of surfactants on the in vitro and in vivo properties of amphotericin B liposome].

Aim: Some surfactants such as DSPE-PEG, Tween 80 and Brij 35 were used to modify the amphotericin B liposome, improve the stability, optimize the tissue distribution and decrease the toxicity of amphotericin B liposome.

Methods: The amphotericin B liposome was prepared by the film-supersound method. The effects of cholesterol and amphotericin B on the encapsulation percentage were studied.

The study on brain targeting of the amphotericin B liposomes.

To improve transporting drugs across the Blood Brain Barrier (BBB) into the brain, RMP-7 was conjugated to the surface of liposomes containing Amphotericin B (AmB) for cerebral inflammation, because it can selectively bound to the B2 receptors on the capillary blood vessel. First, RMP-7 was conjugated to DSPE-PEG-NHS [1,2-dioleoyl-sn-glycero-3-phosphoethanolamine-n-[poly (ethylenegly-col)]-hydroxy succinamide, PEG M 3400] under mild condition to obtain a predominantly 1:1 conjugate (DSPE-PEG-RMP-7), as evidenced by the Matrix-Assisted Laser Desorption-Ionization Time-of-Flight Mass Spectrometry (MALDI-TOF-MS). The second, endothelium cell was cultured on the cell insert to form an in vitro BBB model and the stereoscan microscope, electric resistance and permeation of horse-radish peroxidase (HRP) across the endothelium cell monolayer were used as indicators to evaluate the integrality of the monolayer, and then the in vitro BBB model was used to determine the bioactivity of DSPE-PEG-RMP-7 "opening" BBB.