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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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.Indonesia graphene sports insole ODM

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.Thailand custom neck pillow ODM

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.Memory foam pillow OEM factory China

📩 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.Soft-touch pillow OEM service in Thailand

Rice University postdoctoral researcher Jie Yang led an effort to adapt Cas13 genome editing tools to serve as a highly sensitive detector for the presence of the SARS-CoV-2 virus, which causes COVID-19. Credit: Jeff Fitlow/Rice University Cas13 Engineered To Simplify the Identification of Coronavirus A new engineered CRISPR-based method accurately finds RNA from SARS-CoV-2, the virus that causes COVID-19. The highly sensitive detector promises to make testing for COVID-19 and other diseases fast and easy. Collaborators at Rice University and the University of Connecticut further engineered the RNA-editing CRISPR-Cas13 system to boost its power for detecting minute amounts of the SARS-CoV-2 virus in biological samples. A huge benefit is that it does this without the time-consuming RNA extraction and amplification step necessary in gold-standard PCR testing. The new platform was highly successful compared to PCR testing. In fact, it found 10 out of 11 positives and no false positives for the virus in tests on clinical samples directly from nasal swabs. The scientists showed their technique finds signs of SARS-CoV-2 in attomolar (10-18) concentrations. The study will be published today (September 22, 2022) in the journal Nature Chemical Biology. It was led by chemical and biomolecular engineer Xue Sherry Gao at Rice’s George R. Brown School of Engineering and postdoctoral researchers Jie Yang of Rice and Yang Song of Connecticut. Using structure-guided Cas13, researchers at Rice University and the University of Connecticut modified a gene editing tool to serve as a highly sensitive diagnostic test for the presence of the SARS-CoV-2 virus. They used an off-the-shelf electrochemical sensor to deliver results. Credit: Jie Yang/Rice University Engineering Cas13 for Improved Sensitivity Cas13, like its better-known cousin Cas9, is part of the system by which bacteria naturally defend themselves against invading phages. Since its discovery, CRISPR-Cas9 has been adapted by scientists to edit living DNA genomes and shows great promise to treat and even cure diseases. And it can be used in other ways. Cas13 on its own can be enhanced with guide RNA to find and snip target RNA sequences, but also to find “collateral,” in this case the presence of viruses like SARS-CoV-2. “The engineered Cas13 protein in this work can be readily adapted to other previously established platforms,” Gao said. “The stability and robustness of engineered Cas13 variants make them more suitable for point-of-care diagnostics in low-resource setting areas when expensive PCR machines are not available.” Yang said wild-type Cas13, drawn from a bacterium, Leptotrichia wadei, cannot detect attomolar level of viral RNA within a time frame of 30 to 60 minutes, but the enhanced version created at Rice does the job in about half an hour and detects SARS-CoV-2 in much lower concentrations than the previous tests. She said the key is a well-hidden, flexible hairpin loop near Cas13’s active site. “It’s in the middle of the protein near the catalytic site that determines Cas13’s activity,” Yang said. “Since Cas13 is large and dynamic, it was challenging to find a site to insert another functional domain.” From left, Rice University undergraduate student Jeffrey Vanegas, chemical and biomolecular engineer Xue Sherry Gao and postdoctoral researcher Jie Yang led the effort to modify a gene editing tool to serve as a diagnostic test for the presence of the SARS-CoV-2 virus. Credit: Rice University The research team fused seven different RNA binding domains to the loop, and two of the complexes were clearly superior. When they found their targets, the proteins would fluoresce, revealing the presence of the virus. Transitioning to an Electrochemical Sensor “We could see the increased activity was five- or six-fold over wild-type Cas13,” Yang said. “This number seems small, but it’s quite astonishing with a single step of protein engineering. “But that was still not enough for detection, so we moved the whole assay from a fluorescence plate reader, which is quite large and not available in low-resource settings, to an electrochemical sensor, which has higher sensitivity and can be used for point-of-care diagnostics,” she said. With the off-the-shelf sensor, Yang said the engineered protein was five orders of magnitude (100,000x) more sensitive in detecting the virus compared to the wild-type protein. The lab wants to adapt its technology to paper strips like those in home COVID-19 antibody tests, but with much higher sensitivity and accuracy. “We hope that will make testing more convenient and with lower cost for many targets,” Gao said. The researchers are also investigating improved detection of the Zika, dengue, and Ebola viruses and predictive biomarkers for cardiovascular disease. Their work could lead to rapid diagnosis of the severity of COVID-19. “Different viruses have different sequences,” Yang said. “We can design guide RNA to target a specific sequence that we can then detect, which is the power of the CRISPR-Cas13 system.” But because the project began just as the COVID-19 pandemic took hold, SARS-CoV-2 was a natural focus. “The technology is quite amenable to all the targets,” she said. “This makes it a very good option to detect all kinds of mutations or different coronaviruses.” “We are very excited about this work as a combinational effort of structure biology, protein engineering, and biomedical device development,” Gao added. “I greatly appreciate all the efforts from my lab members and collaborators.” Reference: “Engineered LwaCas13a with enhanced collateral activity for nucleic acid detection” by Jie Yang, Yang Song, Xiangyu Deng, Jeffrey A. Vanegas, Zheng You, Yuxuan Zhang, Zhengyan Weng, Lori Avery, Kevin D. Dieckhaus, Advaith Peddi, Yang Gao, Yi Zhang and Xue Gao, 22 September 2022, Nature Chemical Biology. DOI: 10.1038/s41589-022-01135-y Co-authors of the paper are Rice postdoctoral researcher Xiangyu Deng, undergraduate Jeffrey Vanegas, and graduate student Zheng You; graduate students Yuxuan Zhang and Zhengyan Weng of the University of Connecticut; microbiology supervisor Lori Avery and Kevin Dieckhaus, a professor of medicine, of UConn Health; Yi Zhang, an assistant professor of biomedical engineering at the University of Connecticut; and Yang Gao, an assistant professor of biosciences at Rice. Xue Sherry Gao is the Ted N. Law Assistant Professor of Chemical and Biomolecular Engineering at Rice. The National Science Foundation (2031242, 2103025), the Welch Foundation (C-1952, C-2033-20200401), and the Cancer Prevention and Research Institute of Texas (RR190046) supported the research.

Researchers at Gladstone Institutes have conducted an analysis of numerous human and chimpanzee HARs and found that a number of the modifications that occurred during human evolution had opposing effects on each other. Many alterations to the genomes of early humans had opposing effects, likely due to a delicate balance between enhanced cognitive abilities and an increased risk of psychiatric disorders. Humans and chimpanzees share 99% of their DNA, with human accelerated regions (HARs) being the portions of the genome that exhibit a disproportionate amount of these differences. These HARs remained unchanged in mammals for millennia but underwent rapid transformation in early humans. Scientists have long wondered about the reason for these significant changes in these segments of DNA and how they distinguish humans from other primates. Recently, the researchers at Gladstone Institutes conducted an analysis of thousands of human and chimpanzee HARs and found that a significant number of the modifications that occurred during human evolution had opposing effects from each other. “This helps answer a longstanding question about why HARs evolved so quickly after being frozen for millions of years,” says Katie Pollard, Ph.D., director of the Gladstone Institute of Data Science and Biotechnology and lead author of the new study published in the journal Neuron. “An initial variation in a HAR might have turned up its activity too much, and then it needed to be turned down.” Sean Whalen (left), Katie Pollard (right), and their colleagues at Gladstone Institutes discover that many changes to the genomes of early humans had opposing effects from each other, possibly because of a delicate balance between improved cognition and psychiatric disease risk. Credit: Michael Short/Gladstone Institutes The findings, she says, have implications for understanding human evolution. In addition—because she and her team discovered that many HARs play roles in brain development—the study suggests that variations in human HARs could predispose people to psychiatric disease. “These results required cutting-edge machine learning tools to integrate dozens of novel datasets generated by our team, providing a new lens to examine the evolution of HAR variants,” says Sean Whalen, Ph.D., first author of the study and senior staff research scientist in Pollard’s lab. Enabled by Machine Learning Pollard discovered HARs in 2006 when comparing the human and chimpanzee genomes. While these stretches of DNA are nearly identical among all humans, they differ between humans and other mammals. Pollard’s lab went on to show that the vast majority of HARs are not genes, but enhancers— regulatory regions of the genome that control the activity of genes. More recently, Pollard’s group wanted to study how human HARs differ from chimpanzee HARs in their enhancer function. In the past, this would have required testing HARs one at a time in mice, using a system that stains tissues when a HAR is active. Instead, Whalen input hundreds of known human brain enhancers, and hundreds of other non-enhancer sequences, into a computer program so that it could identify patterns that predicted whether any given stretch of DNA was an enhancer. Then he used the model to predict that a third of HARs control brain development. “Basically, the computer was able to learn the signatures of brain enhancers,” says Whalen. Knowing that each HAR has multiple differences between humans and chimpanzees, Pollard and her team questioned how individual variants in a HAR impacted its enhancer strength. For instance, if eight nucleotides of DNA differed between a chimpanzee and human HAR, did all eight have the same effect, either making the enhancer stronger or weaker? “We’ve wondered for a long time if all the variants in HARs were required for it to function differently in humans, or if some changes were just hitchhiking along for the ride with more important ones,” says Pollard, who is also chief of the division of bioinformatics in the Department of Epidemiology and Biostatistics at UC San Francisco (UCSF), as well as a Chan Zuckerberg Biohub investigator. To test this, Whalen applied a second machine learning model, which was originally designed to determine if DNA differences from person to person affect enhancer activity. The computer predicted that 43 percent of HARs contain two or more variants with large opposing effects: some variants in a given HAR made it a stronger enhancer, while other changes made the HAR a weaker enhancer. This result surprised the team, who had expected that all changes would push the enhancer in the same direction, or that some “hitchhiker” changes would have no impact on the enhancer at all. Measuring HAR Strength To validate this compelling prediction, Pollard collaborated with the laboratories of Nadav Ahituv, Ph.D., and Alex Pollen, Ph.D., at UCSF. The researchers fused each HAR to a small DNA barcode. Each time a HAR was active, enhancing the expression of a gene, the barcode was transcribed into a piece of RNA. Then, the researchers used RNA sequencing technology to analyze how much of that barcode was present in any cell—indicating how active the HAR had been in that cell. “This method is much more quantitative because we have exact barcode counts instead of microscopy images,” says Ahituv. “It’s also much higher throughput; we can look at hundreds of HARs in a single experiment.” When the group carried out their lab experiments on over 700 HARs in precursors to human and chimpanzee brain cells, the data mimicked what the machine learning algorithms had predicted. “We might not have discovered human HAR variants with opposing effects at all if the machine learning model hadn’t produced these startling predictions,” said Pollard. Implications for Understanding Psychiatric Disease The idea that HAR variants played tug-of-war over enhancer levels fits in well with a theory that has already been proposed about human evolution: that the advanced cognition in our species is also what has given us psychiatric diseases. “What this kind of pattern indicates is something called compensatory evolution,” says Pollard. “A large change was made in an enhancer, but maybe it was too much and led to harmful side effects, so the change was tuned back down over time—that’s why we see opposing effects.” If initial changes to HARs led to increased cognition, perhaps subsequent compensatory changes helped tune back down the risk of psychiatric diseases, Pollard speculates. Her data, she adds, can’t directly prove or disprove that idea. But in the future, a better understanding of how HARs contribute to psychiatric disease could not only shed light on evolution but on new treatments for these diseases. “We can never wind the clock back and know exactly what happened in evolution,” says Pollard. “But we can use all these scientific techniques to simulate what might have happened and identify which DNA changes are most likely to explain unique aspects of the human brain, including its propensity for psychiatric disease.” Reference: “Machine learning dissection of human accelerated regions in primate neurodevelopment” by Sean Whalen, Fumitaka Inoue, Hane Ryu, Tyler Fair, Eirene Markenscoff-Papadimitriou, Kathleen Keough, Martin Kircher, Beth Martin, Beatriz Alvarado, Orry Elor, Dianne Laboy Cintron, Alex Williams, Md. Abul Hassan Samee, Sean Thomas, Robert Krencik, Erik M. Ullian, Arnold Kriegstein, John L. Rubenstein, Jay Shendure, Alex A. Pollen and Katherine S. Pollard, 13 January 2023, Neuron. DOI: 10.1016/j.neuron.2022.12.026 The study was funded by the Schmidt Futures Foundation and the National Institutes of Health.

Scientists have discovered a brain gene linked to anxiety symptoms, offering a potential new drug target. They found that a molecule, miR483-5p, suppresses another gene, Pgap2, which causes anxiety-related changes in the brain, suggesting a potential mechanism for anxiety relief. This discovery could lead to more effective treatments for anxiety disorders. An international team of scientists has identified a gene in the brain linked to anxiety symptoms, with modifications to this gene shown to reduce anxiety levels. A gene in the brain driving anxiety symptoms has been identified by an international team of scientists. Critically, modification of the gene is shown to reduce anxiety levels, offering an exciting novel drug target for anxiety disorders. The discovery, led by researchers at the Universities of Bristol and Exeter, was published on April 25 in the journal Nature Communications. Anxiety disorders are common with 1 in 4 people diagnosed with a disorder at least once in their lifetime. Severe psychological trauma can trigger genetic, biochemical, and morphological changes in neurons in the brain’s amygdala — the brain region implicated in stress-induced anxiety, leading to the onset of anxiety disorders, including panic attacks and post-traumatic stress disorder. However, the efficacy of currently available anti-anxiety drugs is low with more than half of patients not achieving remission following treatment. Limited success in developing potent anxiolytic (anti-anxiety) drugs is a result of our poor understanding of the neural circuits underlying anxiety and molecular events resulting in stress-related neuropsychiatric states. Uncovering Molecular Events Behind Anxiety In this study, scientists sought to identify the molecular events in the brain that underpin anxiety. They focused on a group of molecules, known as miRNAs in animal models. This important group of molecules, also found in the human brain, regulates multiple target proteins controlling the cellular processes in the amygdala. Following acute stress, the team found an increased amount of one type of molecule called miR483-5p in a mouse amygdala. Importantly, the team showed that increased miR483-5p suppressed the expression of another gene, Pgap2, which in turn drives changes to neuronal morphology in the brain and behavior associated with anxiety. Together, the researchers showed that miR-483-5p acts as a molecular brake that offsets stress-induced amygdala changes to promote anxiety relief. The discovery of a novel amygdala miR483-5p/Pgap2 pathway through which the brain regulates its response to stress is the first stepping stone towards the discovery of novel, more potent, and much-needed treatments for anxiety disorders that will enhance this pathway. Dr. Valentina Mosienko, one of the study’s lead authors and an MRC Fellow and Lecturer in Neuroscience in Bristol’s School of Physiology, Pharmacology and Neuroscience, said: “Stress can trigger the onset of a number of neuropsychiatric conditions that have their roots in an adverse combination of genetic and environmental factors. While low levels of stress are counterbalanced by the natural capacity of the brain to adjust, severe or prolonged traumatic experiences can overcome the protective mechanisms of stress resilience, leading to the development of pathological conditions such as depression or anxiety. “miRNAs are strategically poised to control complex neuropsychiatric conditions such as anxiety. But the molecular and cellular mechanisms they use to regulate stress resilience and susceptibility were until now, largely unknown. The miR483-5p/Pgap2 pathway we identified in this study, activation of which exerts anxiety-reducing effects, offers a huge potential for the development of anti-anxiety therapies for complex psychiatric conditions in humans.” Reference: “miR-483-5p offsets functional and behavioural effects of stress in male mice through synapse-targeted repression of Pgap2 in the basolateral amygdala” by Mariusz Mucha, Anna E. Skrzypiec, Jaison B. Kolenchery, Valentina Brambilla, Satyam Patel, Alberto Labrador-Ramos, Lucja Kudla, Kathryn Murrall, Nathan Skene, Violetta Dymicka-Piekarska, Agata Klejman, Ryszard Przewlocki, Valentina Mosienko and Robert Pawlak, 25 April 2023, Nature Communications. DOI: 10.1038/s41467-023-37688-2 The research was funded by the Medical Research Council, Academy of Medical Sciences, Leverhulme Trust, Marie Sklodowska-Curie, and the Polish National Science Centre.

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