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"Sun, Ji"
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TXNIP: A key protein in the cellular stress response pathway and a potential therapeutic target
Thioredoxin-interacting protein (TXNIP), which is also known as thioredoxin-binding protein 2 (TBP2), directly interacts with the major antioxidant protein thioredoxin (TRX) and inhibits its antioxidant function and expression. However, recent studies have demonstrated that TXNIP is a multifunctional protein with functions beyond increasing intracellular oxidative stress. TXNIP activates endoplasmic reticulum (ER) stress-mediated nucleotide-binding oligomerization domain (NOD)-like receptor protein-3 (NLRP3) inflammasome complex formation, triggers mitochondrial stress-induced apoptosis, and stimulates inflammatory cell death (pyroptosis). These newly discovered functions of TXNIP highlight its role in disease development, especially in response to several cellular stress factors. In this review, we provide an overview of the multiple functions of TXNIP in pathological conditions and summarize its involvement in various diseases, such as diabetes, chronic kidney disease, and neurodegenerative diseases. We also discuss the potential of TXNIP as a therapeutic target and TXNIP inhibitors as novel therapeutic drugs for treating these diseases.
Metabolism: A protein target for diverse disorders
A protein with the potential to fuel uncontrolled inflammation and cell death could offer a target for a variety of metabolic, neurodegenerative, and other diseases. The cellular redox system is a set of reactions that helps prevent accumulation of toxic byproducts of metabolism. Stressful conditions lead to the activation of the TXNIP protein, an inhibitor of the redox system, and Eui-Hwan Choi and Sun-Ji Park at the Daegu-Gyeongbuk Medical Innovation Foundation, South Korea, have reviewed how TXNIP contributes to diverse pathophysiological states. For example, TXNIP-mediated redox inhibition is associated with the nervous system inflammation seen in Alzheimer’s disease, and also contributes to premature death of insulin-secreting cells in patients with diabetes. Several drugs have been identified that can reduce TXNIP activity, and ongoing preclinical studies are now examining the therapeutic potential of such agents.
Journal Article
Make : tech DIY. Easy electronics projects for parents and kids /
\"Make: Tech DIY introduces younger children to the magic of electronics through the softer side of circuits! Young explorers will learn about electronics through sewing and craft projects aimed at maker parents and their children, elementary school teachers, and kids' activity leaders. Each project introduces new skills and new components in a progressive series of projects that take learners from the very basics to understanding how to use components such as sensors, transistors, and timers.\"--Amazon.com.
Book
Implementation and Evaluation of a Virtual Reality Simulation: Intravenous Injection Training System
In nursing education, virtual reality simulation (VRS) is recognized as an effective learning method as it overcomes limitations in practical training and positively influences learning ability and satisfaction levels. The purpose of this study was to develop VRS for intravenous (IV) injection and investigate how it affects nursing students’ academic knowledge, performance confidence, and clinical practice competencies. A quasi-experimental control group pretest and post-test design was used. Participants were nursing students who either received a training system for an IV injection through VRS (experimental group; n = 20) or who received an IV arm simulator (control group; n = 20). The results revealed significantly higher knowledge (U = 156.5, p = 0.024) and clinical performance competency (U = 87.5, p = 0.002) with the procedure of using a training system of VRS for IV injection compared to having training via an IV arm simulator. This study verified that VRS for IV injection was more effective than an IV arm simulator for practical training on IV injection. Thus, VRS for IV injection, an effective teaching method used to improve learning ability and satisfaction levels, can be used as a training method in the future.
Journal Article
Linsitinib inhibits IGF-1-induced cell proliferation and hyaluronic acid secretion by suppressing PI3K/Akt and ERK pathway in orbital fibroblasts from patients with thyroid-associated ophthalmopathy
Thyroid-associated ophthalmopathy (TAO), an autoimmune disorder of the retrobulbar tissue, is present in up to 50 percent of Graves’s hyperthyroidism patients. Insulin-like growth factor 1 receptor (IGF-1R) has received attention as a target for the development of therapeutic agent for TAO. IGF-1R and TSHR (thyroid stimulating hormone receptor) interact with each other to form a physical or functional complex, further promoting the development of TAO. Linsitinib, OSI-906, is an inhibitor of IGF-1R and has been reported to inhibit cell proliferation of several tumor cells. Linsitinib has been receiving attention not only for its anticancer effect, but also for its anti-inflammatory effects. It has been reported that linsitinib reduces infiltration of inflammatory cells in orbital tissues, resulting in the reduction of muscle edema and adipose tissues in an experimental murine model for Graves’ disease. In the current study, we investigated the issue of whether linsitinib inhibits the IGF-1-induced proliferation of orbital fibroblasts (OFs) via the suppression of phosphatidylinositol 3-kinase (PI3K) / Akt and extracellular signal-regulated kinase (ERK) pathway. Our results showed that pretreatment with linsitinib inhibited IGF-1-induced cell proliferation and hyaluronic acid secretion in the OFs of TAO patients. In addition, our results showed that pretreatment with linsitinib inhibited IGF-1-induced phosphorylation of IGF-1Rβ at Tyr1135, Akt at Ser473, and ERK in the OFs of patients with TAO. These results indicate that linsitinib inhibits IGF-1-induced cell proliferation and hyaluronic acid secretion in the OFs of TAO patients by suppressing the PI3K/Akt and ERK pathways, validating the use of linsitinib as a novel therapeutic agent for TAO.
Journal Article
Unconventional immune cells in the gut mucosal barrier: regulation by symbiotic microbiota
The mammalian gut is the most densely colonized organ by microbial species, which are in constant contact with the host throughout life. Hosts have developed multifaceted cellular and molecular mechanisms to distinguish and respond to benign and pathogenic bacteria. In addition to relatively well-characterized innate and adaptive immune cells, a growing body of evidence shows additional important players in gut mucosal immunity. Among them, unconventional immune cells, including innate lymphoid cells (ILCs) and unconventional T cells, are essential for maintaining homeostasis. These cells rapidly respond to bacterial signals and bridge the innate immunity and adaptive immunity in the mucosal barrier. Here, we focus on the types and roles of these immune cells in physiological and pathological conditions as prominent mechanisms by which the host immune system communicates with the gut microbiota in health and diseases.
Bridging the gap: immunity and gut microbiota
This study highlights the essential role of microbiota in regulating the maintenance and function of ILC subsets and unconventional T cells in the gut. Microbial colonization influences cytokine production, affecting ILC function in barrier maintenance and protection against pathogens. Additionally, microbiota-derived antigens shape MAIT and iNKT cell populations, with their activity finely regulated by a combination of metabolites and local cytokines influenced by the microbiota. Understanding these interactions could lead to innovative strategies for enhancing gut health and effectively treating immune-mediated diseases.
Journal Article
Targeting Mitochondrial Dysfunction and Reactive Oxygen Species for Neurodegenerative Disease Treatment
Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the most common neurodegenerative diseases, and they affect millions of people worldwide, particularly older individuals. Therefore, there is a clear need to develop novel drug targets for the treatment of age-related neurodegenerative diseases. Emerging evidence suggests that mitochondrial dysfunction and reactive oxygen species (ROS) generation play central roles in the onset and progression of neurodegenerative diseases. Mitochondria are key regulators of respiratory function, cellular energy adenosine triphosphate production, and the maintenance of cellular redox homeostasis, which are essential for cell survival. Mitochondrial morphology and function are tightly regulated by maintaining a balance among mitochondrial fission, fusion, biogenesis, and mitophagy. In this review, we provide an overview of the main functions of mitochondria, with a focus on recent progress highlighting the critical role of ROS−induced oxidative stress, dysregulated mitochondrial dynamics, mitochondrial apoptosis, mitochondria-associated inflammation, and impaired mitochondrial function in the pathogenesis of age-related neurodegenerative diseases, such as AD and PD. We also discuss the potential of mitochondrial fusion and biogenesis enhancers, mitochondrial fission inhibitors, and mitochondria-targeted antioxidants as novel drugs for the treatment of these diseases.
Journal Article
Diabetic Retinopathy (DR): Mechanisms, Current Therapies, and Emerging Strategies
Diabetic retinopathy (DR) is one of the most prevalent complications of diabetes, affecting nearly one-third of patients with diabetes mellitus and remaining a leading cause of blindness worldwide. Among the various diabetes-induced complications, DR is of particular importance due to its direct impact on vision and the irreversible damage to the retina. DR is characterized by multiple pathological processes, primarily a hyperglycemia-induced inflammatory response and oxidative stress. Current gold standard therapies, such as anti-VEGF injections and photocoagulation, have shown efficacy in slowing disease progression. However, challenges such as drug resistance, partial therapeutic responses, and the reliance on direct eye injections—which often result in low patient compliance—remain unresolved. This review provides a comprehensive overview of the underlying molecular mechanisms in DR, the current therapies, and their unmet needs for DR treatment. Additionally, emerging therapeutic strategies for improving DR treatment outcomes are discussed.
Journal Article
Chemical Characterization of Kraft Lignin Prepared from Mixed Hardwoods
Chemical characterization of kraft lignin (KL) from mixed hardwoods (Acacia spp. from Vietnam and mixed hardwoods (mainly Quercus spp.) from Korea) was conducted for its future applications. To compare the structural changes that occurred in KL, two milled wood lignins (MWLs) were prepared from the same hardwood samples used in the production of KL. Elemental analysis showed that the MWL from acacia (MWL-aca) and mixed hardwood (MWL-mhw) had almost similar carbon content, methoxyl content, and C9 formula. KL had high carbon content but low oxygen and methoxyl contents compared to MWLs. The C9 formula of KL was determined to be C9H7.29O2.26N0.07S0.12(OCH3)1.24. The Mw of KL and MWLs was about 3000 Da and 12,000–13,000 Da, respectively. The structural features of KL and MWLs were investigated by Fourier transform infrared spectroscopy (FT-IR) and nuclear magnetic resonance spectrometry (1H, 13C NMR). The analyses indicated that KL underwent severe structural modifications, such as γ-carbon cleavage, demethylation, and polycondensation reactions during kraft pulping, which resulted in increased aromatic content and decreased aliphatic content. The main linkages in lignin, β-O-4 moieties, were hardly detected in the analysis as these linkages were extensively cleaved by nucleophilic attack of SH- and OH- during pulping.
Journal Article