Introduction – Company Background

GuangXin Industrial Co., Ltd. is a specialized manufacturer dedicated to the development and production of high-quality insoles.

With a strong foundation in material science and footwear ergonomics, we serve as a trusted partner for global brands seeking reliable insole solutions that combine comfort, functionality, and design.

With years of experience in insole production and OEM/ODM services, GuangXin has successfully supported a wide range of clients across various industries—including sportswear, health & wellness, orthopedic care, and daily footwear.

From initial prototyping to mass production, we provide comprehensive support tailored to each client’s market and application needs.

At GuangXin, we are committed to quality, innovation, and sustainable development. Every insole we produce reflects our dedication to precision craftsmanship, forward-thinking design, and ESG-driven practices.

By integrating eco-friendly materials, clean production processes, and responsible sourcing, we help our partners meet both market demand and environmental goals.

Core Strengths in Insole Manufacturing

At GuangXin Industrial, our core strength lies in our deep expertise and versatility in insole and pillow manufacturing. We specialize in working with a wide range of materials, including PU (polyurethane), natural latex, and advanced graphene composites, to develop insoles and pillows that meet diverse performance, comfort, and health-support needs.

Whether it's cushioning, support, breathability, or antibacterial function, we tailor material selection to the exact requirements of each project-whether for foot wellness or ergonomic sleep products.

We provide end-to-end manufacturing capabilities under one roof—covering every stage from material sourcing and foaming, to precision molding, lamination, cutting, sewing, and strict quality control. This full-process control not only ensures product consistency and durability, but also allows for faster lead times and better customization flexibility.

With our flexible production capacity, we accommodate both small batch custom orders and high-volume mass production with equal efficiency. Whether you're a startup launching your first insole or pillow line, or a global brand scaling up to meet market demand, GuangXin is equipped to deliver reliable OEM/ODM solutions that grow with your business.

Customization & OEM/ODM Flexibility

GuangXin offers exceptional flexibility in customization and OEM/ODM services, empowering our partners to create insole products that truly align with their brand identity and target market. We develop insoles tailored to specific foot shapes, end-user needs, and regional market preferences, ensuring optimal fit and functionality.

Our team supports comprehensive branding solutions, including logo printing, custom packaging, and product integration support for marketing campaigns. Whether you're launching a new product line or upgrading an existing one, we help your vision come to life with attention to detail and consistent brand presentation.

With fast prototyping services and efficient lead times, GuangXin helps reduce your time-to-market and respond quickly to evolving trends or seasonal demands. From concept to final production, we offer agile support that keeps you ahead of the competition.

Quality Assurance & Certifications

Quality is at the heart of everything we do. GuangXin implements a rigorous quality control system at every stage of production—ensuring that each insole meets the highest standards of consistency, comfort, and durability.

We provide a variety of in-house and third-party testing options, including antibacterial performance, odor control, durability testing, and eco-safety verification, to meet the specific needs of our clients and markets.

Our products are fully compliant with international safety and environmental standards, such as REACH, RoHS, and other applicable export regulations. This ensures seamless entry into global markets while supporting your ESG and product safety commitments.

ESG-Oriented Sustainable Production

At GuangXin Industrial, we are committed to integrating ESG (Environmental, Social, and Governance) values into every step of our manufacturing process. We actively pursue eco-conscious practices by utilizing eco-friendly materials and adopting low-carbon production methods to reduce environmental impact.

To support circular economy goals, we offer recycled and upcycled material options, including innovative applications such as recycled glass and repurposed LCD panel glass. These materials are processed using advanced techniques to retain performance while reducing waste—contributing to a more sustainable supply chain.

We also work closely with our partners to support their ESG compliance and sustainability reporting needs, providing documentation, traceability, and material data upon request. Whether you're aiming to meet corporate sustainability targets or align with global green regulations, GuangXin is your trusted manufacturing ally in building a better, greener future.

Let’s Build Your Next Insole Success Together

Looking for a reliable insole manufacturing partner that understands customization, quality, and flexibility? GuangXin Industrial Co., Ltd. specializes in high-performance insole production, offering tailored solutions for brands across the globe. Whether you're launching a new insole collection or expanding your existing product line, we provide OEM/ODM services built around your unique design and performance goals.

From small-batch custom orders to full-scale mass production, our flexible insole manufacturing capabilities adapt to your business needs. With expertise in PU, latex, and graphene insole materials, we turn ideas into functional, comfortable, and market-ready insoles that deliver value.

Contact us today to discuss your next insole project. Let GuangXin help you create custom insoles that stand out, perform better, and reflect your brand’s commitment to comfort, quality, and sustainability.

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High-performance graphene insole OEM factory Taiwan

Are you looking for a trusted and experienced manufacturing partner that can bring your comfort-focused product ideas to life? GuangXin Industrial Co., Ltd. is your ideal OEM/ODM supplier, specializing in insole production, pillow manufacturing, and advanced graphene product design.

With decades of experience in insole OEM/ODM, we provide full-service manufacturing—from PU and latex to cutting-edge graphene-infused insoles—customized to meet your performance, support, and breathability requirements. Our production process is vertically integrated, covering everything from material sourcing and foaming to molding, cutting, and strict quality control.Thailand OEM/ODM hybrid insole services

Beyond insoles, GuangXin also offers pillow OEM/ODM services with a focus on ergonomic comfort and functional innovation. Whether you need memory foam, latex, or smart material integration for neck and sleep support, we deliver tailor-made solutions that reflect your brand’s values.

We are especially proud to lead the way in ESG-driven insole development. Through the use of recycled materials—such as repurposed LCD glass—and low-carbon production processes, we help our partners meet sustainability goals without compromising product quality. Our ESG insole solutions are designed not only for comfort but also for compliance with global environmental standards.Private label insole and pillow OEM production factory

At GuangXin, we don’t just manufacture products—we create long-term value for your brand. Whether you're developing your first product line or scaling up globally, our flexible production capabilities and collaborative approach will help you go further, faster.Taiwan anti-bacterial pillow ODM production factory

📩 Contact us today to learn how our insole OEM, pillow ODM, and graphene product design services can elevate your product offering—while aligning with the sustainability expectations of modern consumers.Indonesia insole ODM service provider

The discovery of DDX53’s link to autism deepens understanding of ASD’s genetic basis, particularly its male bias, and highlights the importance of the X chromosome in the condition. Variants in DDX53 and other X-linked genes offer genetic insights into the higher prevalence of ASD in males. A recent study published in The American Journal of Human Genetics has uncovered a previously unknown genetic link to autism spectrum disorder (ASD). Researchers identified that variants in the DDX53 gene, located on the X chromosome, contribute to ASD, shedding new light on the genetic factors underlying the condition. ASD is a group of neurodevelopmental disorders characterized by challenges in communication, social interactions, and behavior. It is more prevalent in males than females. Although the DDX53 gene is known for its role in brain development and function, this study is the first to establish a definitive connection between DDX53 variants and autism. The research, conducted by teams at The Hospital for Sick Children (SickKids) in Canada and the Istituto Giannina Gaslini in Italy, involved clinical testing of 10 individuals with ASD from 8 different families. The results revealed that variants in DDX53 were maternally inherited and present in these individuals, with the majority being male. This finding underscores the potential role of DDX53 in the male predominance observed in ASD. “By pinpointing DDX53 as a key player, particularly in males, we can better understand the biological mechanisms at play and improve diagnostic accuracy for individuals and their families,” says senior author Dr. Stephen Scherer, Senior Scientist, Genetics & Genome Biology and Chief of Research at SickKids, and Director of the McLaughlin Centre at the University of Toronto. “Identifying this new gene as a confirmed contributor to ASD underscores the complexity of autism and the need for comprehensive genetic analysis.” Additional Genetic Insights At the same location on the X chromosome, the researchers found evidence that another gene, PTCHD1-AS, might be involved in autism. The study highlights a case where a boy and his mother, both with autism with little support needs, had a specific gene deletion involving the DDX53 gene and parts of PTCHD1-AS. The study cohort was assembled through an international collaborative effort, involving several renowned clinical and research institutions from Canada, Italy and the U.S. Further analysis of large autism research databases, including Autism Speaks MSSNG and Simons Foundation Autism Research Initiative, identified 26 more individuals with ASD who had similar rare DDX53 variants to the study participants. “This gene has long eluded us, not previously linked to any neuropsychiatric condition. Our findings support a direct link between DDX53 and autism, which is not only crucial for future clinical genetic testing, but its discovery suggests that the pathway it affects is related to the behavioral traits of autism, opening a whole new area of exploration,” says lead author Dr. Marcello Scala, researcher in Medical Genetics at the Istituto Giannina Gaslini, affiliated with the University of Genoa (Department of Neuroscience). In another paper published in the same journal, Scherer and lead author Dr. Marla Mendes, a research fellow at SickKids, identified 59 genetic variants on the X chromosome significantly associated with ASD. The variants were found in genes linked to autism, including PTCHD1-AS (near to DDX53), DMD, HDAC8, PCDH11X, and PCDH19 beside novel ASD-linked candidates ASB11 and ASB9. Additionally, the FGF13 gene was highlighted as being related to ASD, with sex-specific differences, adding more evidence to the role of sex chromosomes in the condition. “These findings provide new insights into the biology of the X chromosome in ASD, providing additional evidence for the involvement of certain genes like DDX53 and FGF13, and suggesting they should be investigated further,” says Scherer. Implications for Autism Research The team notes that the absence of a gene similar to DDX53 in commonly used mouse models may require future researchers to reconsider how they study ASD. Since it lacks a functional equivalent in these models, findings in DDX53 cannot be easily replicated. “Insights from this study could significantly influence the design and interpretation of autism research, particularly in developing new models. Identifying these variants is an important step towards developing more precise diagnostics and therapeutics for patients and families with ASD,” says Scherer. Scherer also added, “both studies provide even more evidence that complex neurobehavioral conditions like autism can sometimes have simple biologic (genetic) underpinnings.” References: “Genetic variants in DDX53 contribute to autism spectrum disorder associated with the Xp22.11 locus” by Marcello Scala, Clarrisa A. Bradley, Jennifer L. Howe, Brett Trost, Nelson Bautista Salazar, Carole Shum, Marla Mendes, Miriam S. Reuter, Evdokia Anagnostou, Jeffrey R. MacDonald, Sangyoon Y. Ko, Paul W. Frankland, Jessica Charlebois, Mayada Elsabbagh, Leslie Granger, George Anadiotis, Verdiana Pullano, Alfredo Brusco, Roberto Keller, Sarah Parisotto, Helio F. Pedro, Laina Lusk, Pamela Pojomovsky McDonnell, Ingo Helbig, Sureni V. Mullegama, Emilie D. Douine, Rosario Ivetth Corona, Bianca E. Russell, Stanley F. Nelson, Claudio Graziano, Maria Schwab, Laurie Simone, Federico Zara and Stephen W. Scherer, 19 December 2024, The American Journal of Human Genetics. DOI: 10.1016/j.ajhg.2024.11.003 “Chromosome X-wide common variant association study in autism spectrum disorder” by Marla Mendes, Desmond Zeya Chen, Worrawat Engchuan, Thiago Peixoto Leal, Bhooma Thiruvahindrapuram, Brett Trost, Jennifer L. Howe, Giovanna Pellecchia, Thomas Nalpathamkalam, Roumiana Alexandrova, Nelson Bautista Salazar, Ethan A. McKee, Natalia Rivera-Alfaro, Meng-Chuan Lai, Sara Bandres-Ciga, Delnaz Roshandel, Clarrisa A. Bradley, Evdokia Anagnostou, Lei Sun and Stephen W. Scherer, 19 December 2024, The American Journal of Human Genetics. DOI: 10.1016/j.ajhg.2024.11.008 The study was funded by the University of Toronto McLaughlin Centre, Autism Speaks, Autism Speaks Canada, Ontario Brain Institute, the Italian Ministry for Education, University and Research and SickKids Foundation. Additional funding was provided by National Institutes of Health and the California Center for Rare Diseases at UCLA.

This microscopy image shows a white blood cell creating a protrusion to reach out to a foreign body. Credit: Virginie Bazin, Claire Hivroz, Julien Husson Like a well-trained soldier, a white blood cell uses specialized abilities to identify and ultimately destroy dangerous intruders, including creating a protrusion to effectively reach out, lock-on, probe, and possibly attack its prey. Researchers reporting in the Biophysical Journal show in detail that these cells take seconds to morph into these highly rigid and viscous defensive units. Senior author Julien Husson, a biophysicist at École Polytechnique near Paris, and collaborators showed previously that certain white blood cells, called T cells, can push and pull perceived threats via specialized connections. To exert such forces, a cell must reorganize its internal structure, making itself more rigid. In the current study, Husson’s team devised a micropipette rheometer to measure the rigidity, along with the viscosity, of a white blood cell during its transformation. The researchers’ goal was to quantify the physical changes that arise in a white blood cell as it pushes or pulls on a foreign body — in this case, a bead coated with chemicals to attract the cell. These videos show a white blood cell creating a protrusion to reach out to a foreign body. Credit: Julien Husson, LadHyX, CNRS, École Polytechnique, Institut Polytec “We knew that when forming and using its protrusion, the cell was strongly reorganizing its cytoskeleton and that this cytoskeleton is a big player in giving a cell its mechanical properties,” says Husson. “So, I believed there should be some signature mechanical trace.” Stiffness is a measure of how much a material deforms when under a certain amount of pressure, whereas viscosity refers to how fast the material deforms under this pressure. Therefore, to simultaneously measure these properties of a white blood cell while instigating the cell’s immune response, the team needed an experimental setup that could somehow both maintain and vary the force on the cell while also causing it to respond as if it come upon a threat. This model shows a white blood cell creating a protrusion to reach out to a foreign body. Credit: Julien Husson The researchers’ solution was to apply a force that carefully oscillated around a constant, average value. The cell’s stiffness was calculated from the tiny deformation induced by the oscillations, and the viscosity was calculated from the delay between an oscillation and resulting deformation. At the same time, the object applying the force was a bead coated with antibodies, which caused the cell to activate, change shape, and latch onto the bead. “Despite expecting some mechanical changes, what we found was surprisingly dramatic,” says Husson. The team looked at three types of white blood cells and discovered that in all cases, “the cells’ stiffnesses and viscosities begin changing within seconds of coming into contact with the beads and increase up to ten times within minutes.” “Intriguingly,” Husson says, “the mechanical changes begin even before any shape changes,” evoking the question of whether these significant changes to white blood cells’ mechanical properties are simply consequences of other functions or have their own utility. The answer to this question could lie in another result of the study: Husson and colleagues found that a cell’s stiffness and viscosity change together, at a fixed ratio that is unique to the cell type, like a mechanical fingerprint. “It was really exciting to know that there was this kind of universality,” he says. Altogether, the paper’s results suggest an underlying physical mechanism that could apply broadly across cell types and lead to new models, theories, and ultimately a better understanding and control of our cells, in our immune system and beyond. Reference: “Rapid viscoelastic changes are a hallmark of early leukocyte activation” by Alexandra Zak, Sara Violeta Merino-Cortés, Anaïs Sadoun, Farah Mustapha, Avin Babataheri, Stéphanie Dogniaux, Sophie Dupré-Crochet, Elodie Hudik, Hai-Tao He, Abdul I. Barakat, Yolanda R. Carrasco and Yannick Ha, 4 May 2021, Biophysical Journal. DOI: 10.1016/j.bpj.2021.02.042 This work was primarily funded by the French National Research Agency, CNRS, École Polytechnique, and the AXA Research Fund.

Fragmentation of mitochondria (green): The Drp-1 proteins responsible for the decay are labeled with antibodies and stained in magenta. Credit: Chair of Virology / University of Wuerzburg A new study reveals that a viral microRNA called miR-aU14 acts as a master switch for reactivating human herpesvirus 6 (HHV-6) from its dormant state. Eight different herpes viruses are known to date in humans. They all settle down permanently in the body after acute infection. Under certain circumstances, they wake up from this dormant phase, multiply, and attack other cells. This reactivation is often associated with symptoms, such as itchy cold sores or shingles. In the course of evolution, most herpesviruses have learned to use small RNA molecules, so-called microRNAs, to reprogram their host cells to their advantage. A research team led by Bhupesh Prusty and Lars Dölken from Julius-Maximilians-Universität (JMU) Würzburg in Bavaria, Germany, has now been able to show for the first time that a viral microRNA acts as a master regulator to induce the reactivation of the virus. In a study published today (May 4, 2022) in the journal Nature, the researchers present the previously unknown cellular mechanism by which human herpesvirus 6 (HHV-6) triggers its own awakening. Problems After Reactivation of the Virus More than 90 percent of all people are infected with HHV-6 without noticing it. The virus probably only causes problems when it wakes up repeatedly. Human herpesvirus 6 (HHV-6) is the common collective name for human betaherpesvirus 6A (HHV-6A) and human betaherpesvirus 6B (HHV-6B). HHV-6A has been described as more neurovirulent, and as such is more frequently found in patients with neuroinflammatory diseases such as multiple sclerosis. HHV-6 (and HHV-7) levels in the brain are also elevated in people with Alzheimer’s disease. HHV-6B primary infection is the cause of the common childhood illness exanthema subitum (also known as roseola infantum or sixth disease). It is passed on from child to child. Adults are unlikely to catch this disease since most people have had it by kindergarten, and once contracted, immunity develops, preventing future reinfection. HHV-6 reactivation is suspected of impairing heart function, causing the rejection of transplanted organs, and triggering diseases such as multiple sclerosis or chronic fatigue syndrome (ME/CFS). In addition, recent studies suggest that this herpesvirus may be involved in the development of schizophrenia, bipolar disorder, and other diseases of the nervous system. “How herpesviruses reactivate from a dormant state is the central question in herpesvirus research,” says JMU virologist Lars Dölken. “If we understand this, we know how to intervene therapeutically.” A previously unknown key to this is a viral microRNA called miR-aU14. It is the central switch that initiates the reactivation of HHV-6. What the microRNA Does in the Cell The regulatory miR-aU14 comes from the virus itself. As soon as it is expressed, it interferes with the metabolism of human microRNAs. In doing so, it selectively interferes with the maturation of several microRNAs of the miR-30 family. As a result, these important cellular microRNAs are no longer produced. This in turn affects a cellular signaling pathway, the so-called miR-30 / p53 / Drp1 axis. Through this pathway, the viral miR-aU14 induces mitochondrial fragmentation. These cell structures are of central importance for energy production, but also for signal transmissions in the defense against viruses. The viral miR-aU14 thus interferes with the production of type I interferons – messenger substances with which the cell signals the presence of viruses to the immune system. Because the interferons are missing, the herpesvirus is able to switch from a dormant to an active state undisturbed. Interestingly, the Würzburg research group was also able to show that the viral microRNA is not only essential for virus replication, but also directly triggers the reactivation of the virus from its dormant state. How the Research Continues The researchers now want to understand the exact mechanism by which the viral microRNA initiates the reactivation of the virus. In addition, there are first indications that other herpesviruses can also be reactivated via the same mechanism. This could reveal therapeutic options to either prevent reactivation of these viruses or to specifically trigger it in order to then eliminate the reactivating cells. Another goal is to understand the molecular consequences of mitochondrial fragmentation in detail. For the first time, this work from Würzburg shows that a microRNA can directly regulate the maturation process of other microRNAs. This also opens up new therapeutic possibilities: Artificial small RNAs can be designed to specifically switch off individual members of microRNA families. Such subtle interventions were not possible until now. Reference: “Selective inhibition of miRNA processing by a herpesvirus-encoded miRNA” by Thomas Hennig, Archana B. Prusty, Benedikt B. Kaufer, Adam W. Whisnant, Manivel Lodha, Antje Enders, Julius Thomas, Francesca Kasimir, Arnhild Grothey, Teresa Klein, Stefanie Herb, Christopher Jürges, Markus Sauer, Utz Fischer, Thomas Rudel, Gunter Meister, Florian Erhard, Lars Dölken and Bhupesh K. Prusty, 4 May 2022, Nature. DOI: 10.1038/s41586-022-04667-4 Cooperation Partners and Sponsors Several groups at JMU are conducting interdisciplinary research on this topic. They come from the Institute of Virology and Immunobiology, the Biocentres’ Chairs of Biochemistry, Biotechnology and Biophysics, and Microbiology, the Rudolf Virchow Centre and the Helmholtz Institute for RNA-based Infection Research. Researchers from the Free University of Berlin and the University of Regensburg were also involved. The research was funded by the Helmholtz Institute for RNA-based Infection Research, the Solve ME/CFS Initiative (USA), the HHV-6 Foundation (USA), the Amar Foundation (USA) and by the European Research Council within the framework of an ERC grant.

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