Development of a predictive model for the progression of Kawasaki disease: a retrospective analysis of clinical and echocardiographic data.

Unlabelled: This study aimed to identify risk factors for the progression of coronary artery lesions (CALs) in children with Kawasaki disease (KD) and to establish a nomogram for predicting this risk. We retrospectively analyzed clinical and echocardiographic data from KD patients diagnosed at Beijing Children's Hospital from 1 January 2021 to 30 December 2023.The patients were categorized into the progression and non-progression groups on the basis of coronary artery Z-scores and diameters at the 1-month follow-up compared with baseline.

Multichannel-optical imaging for in vivo evaluating the safety and therapeutic efficacy of stem cells in tumor model in terms of cell tropism, proliferation and NF-κB activity.

Stem cell-based cancer treatment has garnered significant attention, yet its safety and efficacy remain incompletely understood. The nuclear factor-kappa B (NF-κB) pathway, a critical signaling mechanism involved in tumor growth, angiogenesis, and invasion, serves as an essential metric for evaluating the behavior of stem cells in tumor models. Herein, we report the development of a triple-channel imaging system capable of simultaneously monitoring the tropism of stem cells towards tumors, assessing tumor proliferation, and quantifying tumor NF-κB activity.

Inhibition of voltage-gated sodium ion channel by corannulene and computational inversion blockage underlying mechanisms.

Corannulene (Cor), a special carbon material, evidenced strong protein binding capacity which regulating lysozyme crystallization and controlling reactive oxygen species (ROS) generation. Ion channel protein play role in regulating ion channel functions to affect physiological functions. However, the interaction between Cor and ion channel protein have not been studied.

Social Deficits and Cerebellar Degeneration in Purkinje Cell Knockout Mice.

Mutations in the gene encoding the voltage-gated sodium channel α-subunit Nav1. 6 have been reported in individuals with epilepsy, intellectual disability and features of autism spectrum disorder. is widely expressed in the central nervous system, including the cerebellum.

TRPC6 interacted with K1.1 channels to regulate the proliferation and apoptosis of glioma cells.

Malignant glioma is the most aggressive and deadliest brain malignancy. TRPC6 and K1.1, two ion channels, have been considered as potential therapeutic targets for malignant glioma treatment.

Reaction-Diffusion Model-Based Research on Formation Mechanism of Neuron Dendritic Spine Patterns.

The pattern abnormalities of dendritic spine, tiny protrusions on neuron dendrites, have been found related to multiple nervous system diseases, such as Parkinson's disease and schizophrenia. The determination of the factors affecting spine patterns is of vital importance to explore the pathogenesis of these diseases, and further, search the treatment method for them. Although the study of dendritic spines is a hot topic in neuroscience in recent years, there is still a lack of systematic study on the formation mechanism of its pattern.

MiR-429/200a/200b negatively regulate Notch1 signaling pathway to suppress CoCl-induced apoptosis in PC12 cells.

Neuronal apoptosis is a central hallmark of cerebral ischemia, which is serious threats to human health. Notch1 signaling pathway and three members of miR-200 family, miR-429, miR-200a and miR-200b, are reported to have tight connection with hypoxia-induced injury. However, their mutual regulation relationship and their roles in neuronal apoptosis caused by hypoxia are rarely reported.

The inhibition of BDNF/TrkB/PI3K/Akt signal mediated by AG1601 promotes apoptosis in malignant glioma.

Malignant glioma is the most aggressive primary brain tumor and has a poor survival rate. Even if extensive methods are preformed to treat glioma, the mortality rate is still very high. It is necessary for discovering and developing new drugs for malignant glioma treatment.

Pretreatment-Etidronate Alleviates CoCl Induced-SH-SY5Y Cell Apoptosis via Decreased HIF-1α and TRPC5 Channel Proteins.

Chronic hypoxic damage is one of the most common pathogenic factors that can cause neurodegenerative disorder in most cases. Etidronate (Eti) is one of the best-known earlier-generations of bisphosphonate derivatives for the treatment of bone-loss related diseases. Building on the preceding study of our laboratory, we found that Eti showed neuroprotective effects against 2-vessel occlusion induced vascular dementia (VD) in rats.

Excessive corticosterone induces excitotoxicity of hippocampal neurons and sensitivity of potassium channels via insulin-signaling pathway.

Corticosterone (CORT) is a kind of corticosteroid produced by cortex of adrenal glands. Hypothalamic-pituitary-adrenal (HPA) axis hyperfunction leads to excessive CORT, which is associated with depression. Few studies have investigated the role of CORT in voltage-gated ion channels and its upstream signaling pathway in central nervous system.

Deletion of asparagine endopeptidase reduces anxiety- and depressive-like behaviors and improves abilities of spatial cognition in mice.

Mammalian asparagine endopeptidase (AEP) is a lysosomal cysteine protease that cleaves protein substrates on the C-terminal side of asparagine. The expression and activity of AEP are closely related to many pathological conditions that include cancer, atherosclerosis and inflammation. It has been validated that the level of AEP is elevated in aged human and neurodegenerative diseases like Alzheimer's disease (AD).

Effects of miR-200b-3p inhibition on the TRPC6 and BK channels of podocytes.

Transient receptor potential canonical 6 (TRPC6) and large-conductance Ca-activated K channels (BK), two of the key ion channels for blood filtration function of podocytes, have been implicated in the pathogenesis of kidney diseases. Moreover, it has been reported that miR-200 b plays an important role in regulating the biological processes of podocytes. In this study, we aimed to examine whether there was a relationship between miR-200 b-3p and the two ion channels.

Voluntary running-enhanced synaptic plasticity, learning and memory are mediated by Notch1 signal pathway in C57BL mice.

It is well known that voluntary running can enhance synaptic plasticity and improve learning and memory abilities. The Notch1 receptor is also reported to be associated with these processes, but its role in running-induced alterations is unclear. In this study, we aimed to investigate whether the Notch1 signalling pathway was involved in voluntary running-induced enhancement of synaptic plasticity, learning and memory.

Angiotensin II induces calcium-mediated autophagy in podocytes through enhancing reactive oxygen species levels.

As well known, abnormalities of Angiotensin II (Ang II) is closely related with glomerular damage. This study was to investigate whether Ang II could affect autophagy in podocytes via oxidative stress, and whether autophagy had a positive role in protecting podocytes impaired by Ang II. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay showed that Ang II induced podocyte death.

Resveratrol Attenuates Aβ-Induced Early Hippocampal Neuron Excitability Impairment via Recovery of Function of Potassium Channels.

Alzheimer's disease (AD) is an age-related neurodegenerative disease. Amyloid-β (Aβ) is not only the morphological hallmark but also the initiator of the pathology process of AD. As a natural compound found in grapes, resveratrol shows a protective effect on the pathophysiology of AD, but the underlying mechanism is not very clear.

Leonurine ameliorates cognitive dysfunction via antagonizing excitotoxic glutamate insults and inhibiting autophagy.

Background: Chronic cerebral hypoperfusion is related with cognitive deficits in different types of dementia.

Purpose: In this study, we aimed to investigate the effect and potential mechanisms of leonurine on chronic cerebral hypoperfusion both in vitro and in vivo.

Study Design: Chronic cerebral hypoperfusion was duplicated by oxygen-glucose deprivation (OGD) in vitro and by ligation of bilateral common carotid arteries (2-VO) in vivo.

Nano-TiO induces autophagy to protect against cell death through antioxidative mechanism in podocytes.

Autophagy is a cellular pathway involved in degradation of damaged organelles and proteins in order to keep cellular homeostasis. It plays vital role in podocytes. Titanium dioxide nanoparticles (nano-TiO) are known to induce autophagy in cells, but little has been reported about the mechanism of this process in podocytes and the role of autophagy in podocyte death.

miR-200 family promotes podocyte differentiation through repression of RSAD2.

Mature podocytes are highly differentiated cells with several characteristic phenotypic features that are involved in the glomerular filtration function. During kidney development, a series of changes of the morphological characteristics and cellular functions may happen in podocytes. The miR-200 family functions in various biological and pathological processes.

Autophagy ameliorates cognitive impairment through activation of PVT1 and apoptosis in diabetes mice.

The underlying mechanisms of cognitive impairment in diabetes remain incompletely characterized. Here we show that the autophagic inhibition by 3-methyladenine (3-MA) aggravates cognitive impairment in streptozotocin-induced diabetic mice, including exacerbation of anxiety-like behaviors and aggravation in spatial learning and memory, especially the spatial reversal memory. Further neuronal function identification confirmed that both long term potentiation (LTP) and depotentiation (DPT) were exacerbated by autophagic inhibition in diabetic mice, which indicating impairment of synaptic plasticity.