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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China OEM/ODM hybrid insole services

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.Graphene insole manufacturer in Vietnam

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.Vietnam eco-friendly graphene material processing

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.China ergonomic pillow OEM supplier

📩 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.Customized sports insole ODM Indonesia

Scientists sequenced near-complete genomes of susceptible and highly insecticide-resistant bed bug strains, uncovering 729 resistance-specific mutations, including genes linked to DNA damage response and cell cycle regulation. These findings could guide more effective pest control strategies and shed light on the evolution of resistance mechanisms. Scientists mapped genomes of bed bug strains, identifying 729 mutations linked to insecticide resistance, offering insights for improved pest control. Scientists have successfully mapped near-complete and highly accurate genomes for two strains of bed bugs: one highly susceptible to insecticides and another “superstrain” that is roughly 20,000 times more resistant. This achievement provides the most comprehensive view yet of the genetic mutations behind insecticide resistance. The findings were published in the journal Insects. While bed bugs are not known to transmit diseases to humans, their bites can cause itchy rashes and secondary infections. Insecticide use, including the now-banned DDT, nearly eradicated bed bug populations by the 1960s, making infestations a rarity. However, over the past two decades, bed bugs have made a global resurgence, largely due to genetic mutations that have rendered them resistant to modern insecticides. Resistance can develop through various mechanisms, such as producing detoxifying enzymes (metabolic resistance) or evolving thicker protective outer layers that block chemicals (penetration resistance). Previous studies have identified some of the genes and mutations involved in resistance, but the complete genetic picture remained unclear because no prior research had sequenced the entire genomes of resistant strains. This new study fills critical gaps, shedding light on the full spectrum of mutations driving their resilience. The number of mutation sites per transcript is shown by circles. (b–g) Mutation sites of candidate resistance genes are shown with different amino acids. “Susceptible” refers to the susceptible strain sequenced in this study and Clec2.1 (pre-existing genome sequence of bed bugs). Gene IDs are indicated by ‘g’ followed by a number, and transcript variations are denoted by ‘t’ followed by a number. In (b), two mutated sites corresponded to the sites of 925 in housefly Musca domestica. Credit: Kouhei Toga/Hiroshima University A research team led by Hidemasa Bono, professor at Hiroshima University’s (HU) Graduate School of Integrated Sciences for Life, mapped genomes of susceptible and resistant bed bug strains from Japan to address this gap. They obtained susceptible strains descended from wild bed bugs (Cimex lectularius) collected 68 years ago in fields at Isahaya City, Nagasaki. Meanwhile, the resistant strains were bred from specimens collected from a Hiroshima City hotel in 2010. Their tests revealed that the resistant samples had 19,859-fold stronger resistance to pyrethroids — the most commonly used insecticide for bed bug control — exceeding levels seen in many previously identified superstrains. All the specimens were provided by Fumakilla Limited, a Japan-based chemical manufacturing company. Piecing together the genome puzzle Sequencing a genome is like assembling a massive jigsaw puzzle, spanning anywhere from about 160,000 to 160 billion pieces. To map the most complete bed bug genomes to date, researchers used the breakthrough method of long-read sequencing, which captures longer stretches of DNA—akin to having entire sections of puzzle pieces put together. Traditional short-read sequencing, by contrast, only covers tiny snippets, often leading to frustrating gaps. The researchers assembled a near-total picture of the two genomes with just about every piece precisely where it belonged, achieving 97.8% completeness and quality value (QV) of 57.0 for the susceptible strain and 94.9% completeness and QV of 56.9 for the resistant strain. A QV above 30 indicates high-quality sequences with less than 0.1% error rate. Both also surpassed the N50 value of the existing C. lectularius reference genome, Clec2.1, from a previous sequencing effort, meaning there were fewer gaps and more complete sections of the genome puzzle. Known, new resistance mutations uncovered After fully sequencing the genomes, the team identified protein-coding genes, determined their functions, and assessed if they were active through transcriptional analysis. They uncovered 3,938 transcripts with amino acid mismatches. Of these, 729 mutated transcripts were linked to insecticide resistance. “We determined the genome sequence of insecticide-resistant bed bugs, which exhibited 20,000-fold greater resistance compared to susceptible bed bugs. By comparing the amino acid sequences between the susceptible and resistant bed bugs, we identified 729 transcripts with resistance-specific mutations,” said study first author Kouhei Toga, postdoctoral researcher at the Laboratory of Genome Informatics of HU’s Graduate School of Integrated Sciences for Life. “These transcripts included genes related to DNA damage response, cell cycle regulation, insulin metabolism, and lysosome functions. This suggests that these molecular pathways may play a role in the development of pyrethroid resistance in bed bugs.” By drawing on previous insect studies, the researchers confirmed known resistance mutations and discovered new ones that could inform more targeted and effective pest control strategies. “We identified a large number of genes likely involved in insecticide resistance, many of which have not been previously reported as being associated with resistance in bedbugs. Genome editing of these genes could provide valuable insights into the evolution and mechanisms of insecticide resistance,” Toga said. “Additionally, this study expands the pool of target genes for monitoring allele distribution and frequency changes, which could contribute significantly to assessing resistance levels in wild populations. This work highlights the potential of genome-wide approaches in understanding insecticide resistance in bed bugs.” Reference: “Genome-Wide Search for Gene Mutations Likely Conferring Insecticide Resistance in the Common Bed Bug, Cimex lectularius” by Kouhei Toga, Fumiko Kimoto, Hiroki Fujii and Hidemasa Bono, 23 September 2024, Insects. DOI: 10.3390/insects15100737 The study was funded by the Japan Science and Technology Agency and the Subsidy for Bioeconomy Industry Creation Support Project (Hiroshima Prefecture). Other research team members include Fumiko Kimoto and Hiroki Fujii, who are employees of Fumakilla Limited.

Mouse one-cell embryo showing two pronuclei: the human version is similar, and their busy preparation for future development remains a mystery. Credit: Perry Lab, University of Bath The finding that some genes are active from the get-go challenges the textbook view that genes don’t become active in human embryos until they are made up of four-to-eight cells, two or three days after fertilization. The newly discovered activity begins at the one-cell stage – far sooner than previously thought – promising to change the way we think about our developmental origins. The research, published recently in the journal Cell Stem Cell, was co-led by Professor Tony Perry at the University of Bath, Dr. Giles Yeo at the University of Cambridge, and Dr. Matthew VerMilyea at Ovation Fertility, US. Using a method called RNA-sequencing, the team applied precision analysis to individual human eggs and one-cell embryos to make a detailed inventory of tell-tale products of gene activity, called RNA transcripts. It revealed that hundreds of genes awaken in human one-cell embryos. Because the gene activity starts small, previous techniques had not been sensitive enough to detect it. But state-of-the art RNA-sequencing used in this study was able to reveal even small changes. “This is the first good look at the beginning of a biological process that we all go through – the transit through the one-cell embryo stage,” said Professor Perry, from the Department of Biology and Biochemistry at Bath. “Without genome awakening, development fails, so it’s a fundamental step.” The team found that many genes activated in one-cell embryos remain switched on until the four-to-eight-cell stage, at which point they are switched off. “It looks as if there is a sort of genetic shift-work in early embryos: the first shift starts soon after fertilization, in one-cell embryos, and a second shift takes over at the eight-cell stage,” said Professor Perry. What human genome awakening tells us At the moment of human fertilization, sperm, and egg genomes – the collection of all of their genes – are inactive: the sperm and egg rely on transcripts produced when they were being formed for instructions that regulate their characteristics. Transcripts provide essential instructions in all cells, and embryo cells are no exception. This means that it is essential for parental (sperm and egg) genomes to awaken in the new embryo. But when and how does this happen? Understanding the process of genome awakening is important: it is a key piece of the jigsaw of development that promises a better understanding of disease, inheritance, and infertility. The scientists found some activated genes that might be expected to play roles in early embryos, but the roles of others were unknown and could point to embryonic events that we don’t yet understand. The team’s findings also shine a light on how the genes are activated. “Although the trigger for activation is thought to come from the egg, it’s not known how; now we know which genes are involved, we can locate their addresses and use molecular techniques to find out,” said Professor Perry. The link with cancer Remarkably, candidates that might trigger gene activation include factors usually associated with cancer, such as some well-known oncogenes. This led the researchers to speculate that the natural, healthy role of factors that are known to misbehave in cancer, is to awaken genes in one-cell embryos. If this proves to be correct, the team’s findings could illuminate events that initiate cancer, providing new diagnostic and preventive opportunities. The findings also have clinical implications for the inheritance of acquired traits, such as obesity: parents who gain weight seem to pass the trait to their kids. It is not known how such acquired traits are transmitted, but altering gene activation after fertilization is a possible mechanism. As Dr Yeo from the Medical Research Council Metabolic Diseases Unit at Cambridge suggests, “If true, we should be able to see this altered gene activation signature at the one-cell stage.” The team also looked at unhealthy one-cell embryos that do not go on to develop, and found that many of their genes fail to activate. Abnormal embryos have been used to evaluate methods of human heritable genome editing, but the new findings suggest they may be inappropriate as a reliable test system. Reference: “Human embryonic genome activation initiates at the one-cell stage” by Maki Asami, Brian Y.H. Lam, Marcella K. Ma, Kara Rainbow, Stefanie Braun, Matthew D. VerMilyea, Giles S.H. Yeo and Anthony C.F. Perry, 21 December 2021, Cell Stem Cell. DOI: 10.1016/j.stem.2021.11.012

Researchers have identified a new mechanism by which misplaced mitochondrial DNA (mtDNA) can cause inflammation, offering potential targets for therapeutic intervention against autoimmune diseases and aging-related inflammation. Credit: SciTechDaily.com Salk scientists outline mouse cell inflammation pathway from mitochondrial stress to leaking endosomes to immune system initiation, revealing new potential therapeutic targets to reduce inflammation in aging and disease. Cells in the human body contain power-generating mitochondria, each with their own mtDNA—a unique set of genetic instructions entirely separate from the cell’s nuclear DNA that mitochondria use to create life-giving energy. When mtDNA remains where it belongs (inside of mitochondria), it sustains both mitochondrial and cellular health—but when it goes where it doesn’t belong, it can initiate an immune response that promotes inflammation. Discovery of mtDNA Misplacement Mechanism Now, Salk scientists and collaborators at UC San Diego have discovered a novel mechanism used to remove improperly functioning mtDNA from inside to outside the mitochondria. When this happens, the mtDNA gets flagged as foreign DNA and activates a cellular pathway normally used to promote inflammation to rid the cell of pathogens, like viruses. The findings, published in Nature Cell Biology today (February 8, 2024), offer many new targets for therapeutics to disrupt the inflammatory pathway and therefore mitigate inflammation during aging and diseases, like lupus or rheumatoid arthritis. Endosomes (magenta) collect around mitochondria (blue) after infection with virus HSV-1, which attacks mtDNA (green) and causes its release. Credit: Salk Institute Mechanism and Therapeutic Implications “We knew that mtDNA was escaping mitochondria, but how was still unclear,” says senior and co-corresponding author Professor Gerald Shadel, director of the San Diego-Nathan Shock Center of Excellence in the Basic Biology of Aging and holder of the Audrey Geisel Chair in Biomedical Science at Salk. “Using imaging and cell biology approaches, we’re able to trace the steps of the pathway for moving mtDNA out of the mitochondria, which we can now try to target with therapeutic interventions to hopefully prevent the resulting inflammation.” One of the ways our cells respond to damage and infection is with what’s known as the innate immune system. While the innate immune response is the first line of defense against viruses, it can also respond to molecules the body makes that simply resemble pathogens—including misplaced mtDNA. This response can lead to chronic inflammation and contribute to human diseases and aging. From left: Gerald Shadel, Laura Newman, and Uri Manor. Credit: Salk Institute Scientists have been working to uncover how mtDNA leaves mitochondria and triggers the innate immune response, but the previously characterized pathways did not apply to the unique mtDNA stress conditions the Salk team was investigating. So, they turned to sophisticated imaging techniques to gather clues as to where and when things were going awry in those mitochondria. Novel Insights and Future Directions “We had a huge breakthrough when we saw that mtDNA was inside of a mysterious membrane structure once it left mitochondria—after assembling all of the puzzle pieces, we realized that structure was an endosome,” says first author Laura Newman, former postdoctoral researcher in Shadel’s lab and current assistant professor at the University of Virginia. “That discovery eventually led us to the realization that the mtDNA was being disposed of and, in the process, some of it was leaking out.” The team discovered a process beginning with a malfunction in mtDNA replication that caused mtDNA-containing protein masses called nucleoids to pile up inside of mitochondria. Noticing this malfunction, the cell then begins to remove the replication-halting nucleoids by transporting them to endosomes, a collection of organelles that sort and send cellular material for permanent removal. The endosome gets overloaded with these nucleoids, springs a leak, and mtDNA is suddenly loose in the cell. The cell flags that mtDNA as foreign DNA—the same way it flags a virus’s DNA—and initiates the DNA-sensing cGAS-STING pathway to cause inflammation. “Using our cutting-edge imaging tools for probing mitochondria dynamics and mtDNA release, we have discovered an entirely novel release mechanism for mtDNA,” says co-corresponding author Uri Manor, former director of the Waitt Advanced Biophotonics Core at Salk and current assistant professor at UC San Diego. “There are so many follow-up questions we cannot wait to ask, like how other interactions between organelles control innate immune pathways, how different cell types release mtDNA, and how we can target this new pathway to reduce inflammation during disease and aging.” The researchers hope to map out more of this complicated mtDNA-disposal and immune-activation pathway, including what biological circumstances—like mtDNA replication dysfunction and viral infection—are required to initiate the pathway and what downstream effects there may be on human health. They also see an opportunity for therapeutic innovation using this pathway, which represents a new cellular target to reduce inflammation. Reference: “Mitochondrial DNA replication stress triggers a pro-inflammatory endosomal pathway of nucleoid disposal” by Laura E. Newman, Sammy Weiser Novak, Gladys R. Rojas, Nimesha Tadepalle, Cara R. Schiavon, Danielle A. Grotjahn, Christina G. Towers, Marie-Ève Tremblay, Matthew P. Donnelly, Sagnika Ghosh, Michaela Medina, Sienna Rocha, Ricardo Rodriguez-Enriquez, Joshua A. Chevez, Ian Lemersal, Uri Manor and Gerald S. Shadel, 8 February 2024, Nature Cell Biology. DOI: 10.1038/s41556-023-01343-1 Other authors include Sammy Weiser Novak, Gladys Rojas, Nimesha Tadepalle, Cara Schiavon, Christina Towers, Matthew Donnelly, Sagnika Ghosh, Sienna Rocha, and Ricardo Rodriguez-Enriquez of Salk; Danielle Grotjahn and Michaela Medina of The Scripps Research Institute; Marie-Ève Tremblay of the University of Victoria in Canada; Joshua Chevez of UC San Diego; and Ian Lemersal of the La Jolla Institute for Immunology. The work was supported by the National Institutes of Health (R01 AR069876, P30AG068635, 1K99GM141482, 1F32GM137580, T32GM007198, 5R00CA245187, and 5R00CA245187-04S1), an Allen-AHA Initiative in Brain Health and Cognitive Impairment award (19PABH134610000H), a National Science Foundation NeuroNex Award (2014862), Chan-Zuckerberg Initiative Imaging Scientist Award, the LIFE Foundation, a George E. Hewitt Foundation for Medical Research Postdoctoral Fellowship, Paul F. Glenn Foundation for Medical Research Postdoctoral Fellowship, Salk Pioneer Fund Postdoctoral Scholar Award, the Waitt Foundation, Yale University School of Medicine Center for Cellular and Molecular Imaging, a Canada Research Chair (Tier 2) in Neurobiology of Aging and Cognition, and a Canada Foundation for Innovation John R. Evans Leaders Fund (grant 39965).

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