Correction: Kim et al. Neuroprotective Effect of Statins in a Rat Model of Chronic Ocular Hypertension. 2021, , 12500.

In the original publication [...

Modulation of TRPV4-mediated TNF-α expression in Müller glia and subsequent RGC apoptosis by statins.

In addition to regulating cholesterol synthesis, statins have neuroprotective effects. Apoptosis of retinal ganglion cells (RGCs) causes a gradual loss of visual function in glaucoma. This study aimed to investigate the neuroprotective effect of statins on the RGC apoptosis induced by activated Müller glia.

The relationship between perceived restorativeness and place attachment for hikers at Jeju Gotjawal Provincial Park in South Korea: the moderating effect of environmental sensitivity.

Objectives: Jeju Gotjawal Provincial Park provides visitors with opportunities for outdoor recreation and informs visitors of the environmental significance of the park's ecosystem. This study attempted to examine how the perceived restorativeness of park visitors influenced their place attachment. In addition, the moderating effect of environmental sensitivity on the hypothesized relationship was explored.

Exploring the Major Factors Affecting Generalized Anxiety Disorder in Korean Adolescents: Based on the 2021 Korea Youth Health Behavior Survey.

(1) Background: Recently, the prevalence of generalized anxiety disorder (GAD) among adolescents has been higher than in adults. Early detection is important for treatment. Accordingly, although various factors affecting adolescents' GAD have been studied, the body of research is fragmented, and an integrated analysis of the influencing factors is needed.

Statins Inhibit the Gliosis of MIO-M1, a Müller Glial Cell Line Induced by TRPV4 Activation.

We characterized Müller cell gliosis induced by the activation of transient receptor potential vanilloid-type 4 (TRPV4) and assessed whether statins could modulate the gliosis. The human Müller cell line, MIO-M1, was used to analyze the gliosis caused by glaucomatous stimulation. To induce Müller gliosis in MIO-M1 cells, GSK101 was used to activate TRPV4, and Müller gliosis was evaluated by analyzing vimentin, nestin, and glial fibrillary acidic protein (GFAP) expression.

Neuroprotective Effect of Statins in a Rat Model of Chronic Ocular Hypertension.

Glaucoma is an optic neuropathy in which the degeneration of retinal ganglion cells (RGCs) results in irreversible vison loss. Therefore, neuroprotection of RGCs from glaucomatous afflictions is crucial for glaucoma treatment. In this study, we aimed to investigate the beneficial effects of statins in the protection of RGCs using a rat model.

Metabolic Control of Sensory Neuron Survival by the p75 Neurotrophin Receptor in Schwann Cells.

We report that the neurotrophin receptor p75 contributes to sensory neuron survival through the regulation of cholesterol metabolism in Schwann cells. Selective deletion of p75 in mouse Schwann cells of either sex resulted in a 30% loss of dorsal root ganglia (DRG) neurons and diminished thermal sensitivity. P75 regulates Schwann cell cholesterol biosynthesis in response to BDNF, forming a co-receptor complex with ErbB2 and activating ErbB2-mediated stimulation of sterol regulatory element binding protein 2 (SREBP2), a master regulator of cholesterol synthesis.

Investigating 'Fear of Missing Out' (FOMO) as an extrinsic motive affecting sport event consumer's behavioral intention and FOMO-driven consumption's influence on intrinsic rewards, extrinsic rewards, and consumer satisfaction.

This study posits that Fear of Missing Out (FOMO) can function as an extrinsic motive stimulating sport event consumption by inducing consumers to overcome leisure constraints. Also, FOMO-driven consumption is proposed to affect consumption experience for being grounded on extrinsic than intrinsic rewards. In Study 1, the moderation of FOMO between intrapersonal and structural constraints and sport media viewing intention are tested.

Statins Suppress TGF-β2-Mediated MMP-2 and MMP-9 Expression and Activation Through RhoA/ROCK Inhibition in Astrocytes of the Human Optic Nerve Head.

Purpose: Matrix metalloproteinases (MMPs) are involved in extracellular matrix (ECM) maintenance and remodeling. The present study aimed to determine whether transforming growth factor (TGF)-β2 regulates MMP-2 and MMP-9 levels and activities in astrocytes derived from the optic nerve head (ONH) and the role of statins in such modulation.

Methods: Primary astrocytes cultured from the lamina cribrosa of human donor ONHs were incubated with three types of statins (5 µg/mL) for 1 hour followed by recombinant TGF-β2 (5 ng/mL) for various periods to test their effects.

A Qualitative Systematic Review of Public-Private Partnership in Promoting Physical Activity.

The purpose of the study is to conduct a comprehensive review of public-private partnership (PPP) literature that pertains to promoting physical activity. A qualitative systematic review guided data search and screening process, and the findings were synthesized and interpreted using a qualitative content analysis method. Literature was searched from 16 academic and 6 gray literature databases.

The Effects of Tai Chi Intervention on Healthy Elderly by Means of Neuroimaging and EEG: A Systematic Review.

Aging is a process associated with a decline in cognitive and motor functions, which can be attributed to neurological changes in the brain. Tai Chi, a multimodal mind-body exercise, can be practiced by people across all ages. Previous research identified effects of Tai Chi practice on delaying cognitive and motor degeneration.

Statins reduce TGF-beta2-modulation of the extracellular matrix in cultured astrocytes of the human optic nerve head.

Statins are cholesterol lowering drugs and have shown beneficial effects on glaucoma. With regard to the mechanism of statin action on glaucoma, we investigated the effects of statins on transforming growth factor-beta 2 (TGF-β2)-induced expression of extracellular matrix (ECM) proteins in human astrocytes of the optic nerve head (ONH) lamina cribrosa (LC). By using primary human ONH astrocytes, we found that both simvastatin and lovastatin inhibited TGF-β2-mediated expression of ECM proteins such as connective tissue growth factor, collagen I, fibronectin, and plasminogen activator inhibitor-1.

Deletion of in Mouse Skeletal Myofibers Induces Muscle Aging-Related Phenotypes in and in .

Sarcopenia, the loss of muscle mass and strength during normal aging, involves coordinate changes in skeletal myofibers and the cells that contact them, including satellite cells and motor neurons. Here we show that the protein -fucosyltransferase 1 gene (), which encodes a glycosyltransferase required for NotchR-mediated cell-cell signaling, has reduced expression in aging skeletal muscle. Moreover, premature postnatal deletion of in skeletal myofibers can induce aging-related phenotypes in within skeletal myofibers and in within satellite cells and within motor neurons via the neuromuscular junction.

In vitro Effects of Prostaglandin Analogs on Cultured Astrocytes Obtained from the Lamina Cribrosa.

Purpose: To evaluate the effects of prostaglandin analogs (PGAs) on cell viability and apoptosis in cultured astrocytes obtained from the lamina cribrosa (LC) of the human optic nerve head (ONH).

Methods: Astrocytes were cultured from LC samples obtained from human donor ONH and treated with three kinds of acid form of PGAs: latanoprost (LAT-A), tafluprost (TAF-A), and bimatoprost (BIM-A) (0.1, 1, 10, 50 and 100 ug/mL).

p75 regulates Purkinje cell firing by modulating SK channel activity through Rac1.

p75 is expressed among Purkinje cells in the adult cerebellum, but its function has remained obscure. Here we report that p75 is involved in maintaining the frequency and regularity of spontaneous firing of Purkinje cells. The overall spontaneous firing activity of Purkinje cells was increased in p75(-/-) mice during the phasic firing period due to a longer firing period and accompanying reduction in silence period than in the wild type.

Brain-derived neurotrophic factor (BDNF) induces polarized signaling of small GTPase (Rac1) protein at the onset of Schwann cell myelination through partitioning-defective 3 (Par3) protein.

Brain-derived neurotrophic factor (BDNF) was shown to play a role in Schwann cell myelination by recruiting Par3 to the axon-glial interface, but the underlying mechanism has remained unclear. Here we report that Par3 regulates Rac1 activation by BDNF but not by NRG1-Type III in Schwann cells, although both ligands activate Rac1 in vivo. During development, active Rac1 signaling is localized to the axon-glial interface in Schwann cells by a Par3-dependent polarization mechanism.

O-fucosylation of muscle agrin determines its ability to cluster acetylcholine receptors.

Protein O-fucosyltransferase 1 (Pofut1) transfers fucose to serine or threonine on proteins, including Notch receptors, that contain EGF repeats with a particular consensus sequence. Here we demonstrate that agrin is O-fucosylated in a Pofut1-dependent manner, and that this glycosylation can regulate agrin function. Fucosylation of recombinant C45 agrin, both active (neural, z8) and inactive (muscle, z0) splice forms, was eliminated when agrin was overexpressed in Pofut1-deficient cells or by mutation of a consensus site for Pofut1 fucosylation (serine 1726 in the EGF4 domain).

Small, nonpeptide p75NTR ligands induce survival signaling and inhibit proNGF-induced death.

Studies showing that neurotrophin binding to p75NTR can promote cell survival in the absence of Trk (tropomyosin-related kinase) receptors, together with recent structural data indicating that NGF may bind to p75NTR in a monovalent manner, raise the possibility that small molecule p75NTR ligands that positively regulate survival might be found. A pharmacophore designed to capture selected structural and physical chemical features of a neurotrophin domain known to interact with p75NTR was applied to in silico screening of small molecule libraries. Small, nonpeptide, monomeric compounds were identified that interact with p75NTR.

Role for activating transcription factor 3 in stress-induced beta-cell apoptosis.

Activating transcription factor 3 (ATF3) is a stress-inducible gene and encodes a member of the ATF/CREB family of transcription factors. However, the physiological significance of ATF3 induction by stress signals is not clear. In this report, we describe several lines of evidence supporting a role of ATF3 in stress-induced beta-cell apoptosis.