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 Vietnam neck support pillow OEM 》offering full-ser |
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Introduction – Company BackgroundGuangXin 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 ManufacturingAt 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 FlexibilityGuangXin 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 & CertificationsQuality 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 ProductionAt 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 TogetherLooking 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. 🔗 Learn more or get in touch: Taiwan high-end foam product OEM/ODM factory 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 sheet OEM supplier Indonesia 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.Taiwan athletic insole OEM production plant 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 pillow ODM development service 📩 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.Innovative pillow ODM solution in Thailand UCLA researchers have discovered a new memory mechanism in the brain that reduces energy costs and enhances memory storage, potentially offering new insights into Alzheimer’s and other memory disorders. UCLA Health research identifies a new memory state called spontaneous persistent inactivity. UCLA Health researchers have identified a process that memories while reducing metabolic costs, even during sleep. This efficient memory is found in a brain region essential for learning and memory, which is also where Alzheimer’s disease originates. The discovery is published in the journal Nature Communications. Does this sound familiar: You go to the kitchen to fetch something, but when you get there, you forget what you wanted. This is your working memory failing. Working memory is defined as remembering some information for a short period while you go about doing other things. We use working memory virtually all the time. Alzheimer’s and dementia patients have working memory deficits and it also shows up in mild cognitive impairment (MCI). Hence, considerable effort has been devoted to understanding the mechanisms by which the vast networks of neurons in the brain create working memory. The Role of the Entorhinal Cortex During working memory tasks, the outermost layer of the brain, known as the neocortex, sends sensory information to deeper regions of the brain, including a central region called the entorhinal cortex, which is crucial for forming memories. Neurons in the entorhinal cortex show a complex array of responses, which have puzzled scientists for a long time and resulted in the 2014 Nobel Prize in medicine, yet the mechanisms governing this complexity are unknown. The entorhinal cortex is where Alzheimer’s disease begins forming. “It’s therefore critical to understand what kind of magic happens in the cortico-entorhinal network, when the neocortex speaks to the entorhinal cortex which turns it into working memory. It could provide an early diagnostic of Alzheimer’s disease and related dementia, and mild cognitive impairment,” said corresponding author Mayank Mehta, a neurophysicist and head of the W. M. Keck Center for Neurophysics and the Center for Physics of Life at UCLA. To crack this problem, Mehta and his coauthors devised a novel approach: a “mathematical microscope.” In the world of physics, mathematical models are commonly used, from Kepler to Newton and Einstein, to reveal amazing things we have never seen or even imagined, such as the inner workings of subatomic particles and the inside of a black hole. Mathematical models are used in brain sciences too, but their predictions are not taken as seriously as in physics. The reason is that in physics, predictions of mathematical theories are tested quantitatively, not just qualitatively. Such quantitatively precise experimental tests of mathematical theories are commonly believed to be unfeasible in biology because the brain is vastly more complex than the physical world. Mathematical theories in physics are very simple, involving very few free parameters and hence precise experimental tests. In contrast, the brain has billions of neurons and trillions of connections, a mathematical nightmare, let alone a highly precise microscope. Simplifying Complex Systems “To tackle this seemingly impossible challenge of devising a simple theory that can still explain the experimental data of memory dynamics in vivo data with high precision, we hypothesized that cortico-entorhinal dialog, and memory magic, will occur even when the subjects are sleeping, or anesthetized,” said Dr. Krishna Choudhary, the lead author of the study. “Just like a car behaves like a car when it’s idling or going at 70 mph.” UCLA researchers then made another large assumption: the dynamics of the entire cortex and the entorhinal cortex during sleep or anesthesia can be captured by just two neurons. These assumptions reduced the problem of billions of neurons’ interactions to just two only free variables – the strength of input from the neocortex to the entorhinal cortex and the strength of recurrent connections within the entorhinal cortex. While this makes the problem mathematically tractable, it raises the obvious question – is it true? “If we test our theory quantitatively on data in vivo, then these are just interesting mathematical games, not a solid understanding of memory-making magic,” said Mehta. The crucial experimental tests of this theory required sophisticated experiments by Dr. Thomas Hahn, a coauthor who is now a professor at Basel University and a clinical psychologist. “The entorhinal cortex is a complicated circuit. To really test the theory we needed experimental techniques that can not only measure the neural activity with high precision, but also determine the precise anatomical identity of the neuron,” said Hahn. Hahn and Dr. Sven Berberich, also a coauthor, measured the membrane potential of identified neurons from the entorhinal cortex in vivo, using whole cell patch clamp technique and then used anatomical techniques to identify the neuron. Simultaneously they measured the activity of the parietal cortex, a part of the neocortex that sends inputs to the entorhinal cortex. “A mathematical theory and sophisticated in vivo data are necessary and cool, but we had to tackle one more challenge – how does one map this simple theory onto complex neural data?” said Mehta. “This required a protracted period of development, to generate a ‘mathematical microscope’ that can directly reveal the inner workings of neurons as they make memory,” said Choudhary. “As far as we know, this has not been done before.” Discovering New Memory States The authors observed that like an ocean wave forming and then crashing onto a shoreline, the signals from the neocortex oscillate between on and off states in intervals while a person or animal sleeps. Meanwhile, the entorhinal cortex acted like a swimmer in the water who can move up when the waveforms and then down when it recedes. The data showed this and the model captured this as well. But using this simple match the model then took a life of its own and discovered a new type of memory state known as spontaneous persistent inactivity, said Mehta. “It’s as if a wave comes in and the entorhinal cortex said, ‘There is no wave! I’m going to remember that recently there was no wave so I am going to ignore this current wave and not respond at all’. This is persistent inactivity” Mehta said. “Alternately, persistent activity occurs when the cortical wave disappears but the entorhinal neurons remember that there was a wave very recently, and continue rolling forward.” While many theories of working memory had shown the presence of persistent activity, which the authors found, the persistent inactivity was something that the model predicted and had never been seen before. “The cool part about persistent inactivity is that it takes virtually no energy, unlike persistent activity, which takes a lot of energy”, said Mehta, “even better, the combination of persistent activity and inactivity more than doubles the memory capacity while cutting down the metabolic energy cost by half.” “All this sounded too good to be true, so we really pushed our mathematical microscope to the limit, into a regime where it was not designed to work,” said Dr. Choudhary. “If the microscope was right, it would continue working perfectly even in unusual situations.” “The math-microscope made a dozen predictions, not just about entorhinal but many other brain regions too. To our complete surprise, the mathematical microscope worked every time,” Mehta continued. “Such near perfect match between the predictions of a mathematical theory and experiments is unprecedented in neuroscience. “This mathematical model that is perfectly matched with experiments is a new microscope,” Mehta continued. “It reveals something that no existing microscope could see without it. No matter how many neurons you have imaged, it would not have revealed any of this. “In fact, metabolic shortcomings are a common feature of many memory disorders,” said Mehta. Mehta’s laboratory is now following up on this work to understand how complex working memory is formed, and what goes wrong in the entorhinal cortex during Alzheimer’s disease, dementia, and other memory disorders.” Reference: “Spontaneous persistent activity and inactivity in vivo reveals differential cortico-entorhinal functional connectivity” by Krishna Choudhary, Sven Berberich, Thomas T. G. Hahn, James M. McFarland and Mayank R. Mehta, 8 May 2024, Nature Communications. DOI: 10.1038/s41467-024-47617-6 Researchers have linked increased numbers of mutations in children to a higher rate of random mutations in sperm cells of the biological father, associated with chemotherapy or rare genetic defects in DNA repair. Scientists have traced the cause of increased numbers of mutations in children to a higher rate of random mutations in sperm cells of the biological father, associated with rare genetic defects in DNA repair or chemotherapy. New research has found that some rare cases of higher genetic mutation rates in children, known as hypermutation, could be linked to the father receiving certain chemotherapy treatments. Researchers from the Wellcome Sanger Institute and their collaborators analyzed over 20,000 families’ genetic information and identified 12 children with between two to seven times more mutations than the general population. The team linked the majority of these to increased mutations in the sperm of the biological father. The research, published today (May 11, 2022) in the journal Nature, shows that just under half of these fathers had been treated with certain types of chemotherapy earlier in life, which could be linked to the increased number of mutations in their sperm cells. While these cases of hypermutation in children are rare, and in the vast majority of children will not lead to genetic disorders, hypermutation will increase the risk of a child having a rare genetic disorder. It is important to investigate this further due to the implications it has for patients who receive chemotherapy and want to have children in the future. If further research confirms the impact of chemotherapy, patients could be offered the opportunity to freeze their sperm before treatment. Genetic Transmission of Mutations Genomes are copied with a very low error rate when they are passed from one generation to the next. Nevertheless, as the human genome contains three billion letters, random mutations in the sperm and the egg are inevitable and pass from the parent to the child. This means that typically every child has around 60 to 70 new mutations that their biological parents don’t have. These mutations are responsible for genetic variation along with many genetic diseases. Around 75 percent of these random mutations come from the father.[1] Most genetic disorders only occur when both copies of an important gene are damaged, resulting in what is known as a recessive disease. If only one copy is damaged, for example, by a new mutation, the remaining functioning copy of the gene will be able to prevent disease. However, a minority of genetic disorders, known as dominant disorders, occur when only one copy of a gene is damaged. It is these dominant disorders that can be caused by a single, random mutation. One of the main factors influencing mutation rate is the age of the parents, with mutations increasing by 1.3 mutations per year in the fathers and 0.4 mutations per year in mothers.[2] If there is a higher number of germline mutations, there is a higher risk of a child being born with a dominant disorder. However, hypermutation in children does not always mean they will have a dominant disorder. In new research, from the Wellcome Sanger Institute and collaborators, scientists used genetic data and family health histories from existing databases to identify children that had unusually high mutation rates, between two and seven times higher than average, to investigate where these might have originated from. The team analyzed data from over 20,000 UK families with children with suspected genetic conditions participating in the Deciphering Developmental Disorders and 100,000 Genomes projects. They found that children with hypermutation were rare among these families. As the number of children with hypermutations was only 12 out of around 20,000, these rates of increased mutations could not have been caused by common exposures, such as smoking, pollution, or common genetic variation. Chemotherapy’s Impact on Sperm Cells For eight of these children the excess mutations could be linked to their father’s sperm. It was possible to investigate in detail seven of the families, where the excess mutations came from the biological father. Two of the fathers had rare recessive genetic variants that impaired DNA repair mechanisms. The other five men had all previously been treated with chemotherapy before conceiving a child. Three of these children had a pattern of mutations characteristic of chemotherapy using platinum-based drugs and the fathers of the other two children had both received chemotherapy with mustard-derived alkylating agents. However, by linking the genetic data to anonymized health data, it could be shown that most fathers and all mothers who had received chemotherapy prior to conceiving a child did not have children with a notable excess of mutations. This study exemplifies the value of linking nationwide genetic data and routine clinical records in secure, anonymized, and trustworthy ways to provide unique insights into unanticipated, but important, questions. Through the efforts of Health Data Research UK and its partners, these kinds of responsible analyses of potential clinical relevance will be easier to perform in the future. While chemotherapy is one of the most effective treatments for cancer, it is widely recognized that it can have disruptive and debilitating side effects. Clinicians take these into account when prescribing this treatment. Future Research Directions and Family Planning Implications If these types of chemotherapy were shown to impact sperm in some patients, this could have clinical implications on treatment plans and family planning. Further research is required to investigate this at a deeper level before changing treatment for cancer in men. It is currently unclear why these types of chemotherapies seem to impact the sperm more than the egg cells. Dr. Joanna Kaplanis, first author and Post-Doctoral Fellow at the Wellcome Sanger Institute, said: “Hypermutation in children, where they have between two and seven times more random mutations than the general population, is rare and therefore cannot be caused by common carcinogens or exposures. Our research analyses over 20,000 families and highlights new causes of these mutations, linking them back to germline mutations in the father’s sperm as well as identifying a new mutational signature. Understanding the impact of these germline mutations in the sperm could help us uncover why some people are more likely to have children with these high rates of random mutations, and help protect against these if they cause disease.” John Danesh, Director of HDR UK Cambridge, who supported the research, said, “Hypermutation in children is an uncommon but important phenomenon that increases the risk of life-altering genetic diseases. By bringing together genetic data at scale, and linking this with routine clinical data like the hospital records of parents, the team has identified new risk factors that may influence future healthcare decisions. This work elegantly demonstrates how work in Health Data Research UK’s Understanding the Causes of Disease Programme is helping to link nationwide genetic data and clinical records in secure, anonymized, and trustworthy ways that provide unique insights into unanticipated, but important questions.” Sir Mark Caulfield, from Queen Mary University of London, and former Chief Scientist at Genomics England, said: “These findings were only possible due to access to whole genomes and linked health record data on the family members from the 100,000 Genomes Project. These findings could really help people with cancer consider family planning.” Professor Matthew Hurles, senior author and Head of Human Genetics at the Wellcome Sanger Institute, said: “Chemotherapy is an incredibly effective treatment for many cancers, but unfortunately it can have some damaging side effects. Our research found a plausible link between two types of chemotherapy and their impact on sperm in a very small number of men. These results require further systematic studies to see if there is a causal link between chemotherapy and sperm mutations, and if there is a way of identifying individuals at risk prior to treatment so they could take family planning measures, such as freezing their sperm prior to treatment. I would also like to thank the families that donated their genetic and health information to make this research possible.” Reference: “Genetic and chemotherapeutic influences on germline hypermutation” by Joanna Kaplanis, Benjamin Ide, Rashesh Sanghvi, Matthew Neville, Petr Danecek, Tim Coorens, Elena Prigmore, Patrick Short, Giuseppe Gallone, Jeremy McRae, Genomics England Research Consortium, Jenny Carmichael, Angela Barnicoat, Helen Firth, Patrick O’Brien, Raheleh Rahbari and Matthew Hurles, 11 May 2022, Nature. DOI: 10.1038/s41586-022-04712-2 Notes “Properties and rates of germline mutations in humans” by Catarina D. Campbell and Evan E. Eichler, 17 May 2013, Trends In Genetics. DOI: 10.1016/j.tig.2013.04.005 “Prevalence and architecture of de novo mutations in developmental disorders” by Deciphering Developmental Disorders Study, 25 January 2017, Nature. DOI: 10.1038/nature21062 Müller glia (green) and their progeny (red) regenerate nerve cells and photoreceptors in a mouse retina. Credit: Ksenia Gnedeva/USC A USC research team discovered that a single genetic signal may be preventing both hearing and vision cells from repairing themselves. By turning off this signal in mice, they triggered cell growth in parts of the ear and eye — a step toward possible future therapies for hearing and vision loss. A new mouse study from the USC Stem Cell lab of Ksenia Gnedeva, PhD, suggests that the same genes may control the regeneration of sensory cells in both the ear and the eye. The research, published today (March 31) in Proceedings of the National Academy of Sciences (PNAS), offers insight into why these cells fail to regenerate in mammals, and how that barrier might be lifted. Unlocking Regeneration in Ear and Eye “The proliferation of progenitor cells in response to injury is a crucial step in the regeneration of sensory receptors, but this process is blocked in the mammalian inner ear and retina. By understanding the genes that enforce this block, we can advance efforts to restore hearing and vision in patients,” said Gnedeva, an assistant professor in the USC Tina and Rick Caruso Department of Otolaryngology – Head and Neck Surgery, and the Department of Stem Cell Biology and Regenerative Medicine at the Keck School of Medicine of USC. The Hippo Pathway: A Cellular Stop Signal The team, led by first authors Eva Jahanshir and Juan Llamas, focused on a network of genes known as the Hippo pathway. This pathway acts as a “stop growing” signal, previously shown by the lab to limit cell proliferation in the developing ear. In this study, the researchers found that the same pathway also suppresses the regrowth of damaged sensory cells in the ears and eyes of adult mice. To test whether they could overcome this barrier, the scientists used a compound developed in their lab that inhibits a key Hippo pathway protein, Lats1/2. When inner ear progenitor cells, known as supporting cells, were exposed to this compound in a Petri dish, they began to multiply in the utricle, a balance-sensing organ. However, the same effect was not observed in the organ of Corti, which is responsible for hearing. The Role of p27Kip1 in Blocking Regeneration The scientists next identified what was blocking this important step towards sensory cell regeneration in the organ of Corti — a gene encoding a protein called p27Kip1 — and showed that this inhibitory protein was also high in the retina. They created a transgenic mouse in which the level of p27Kip1 could be reduced in the inner ear and the retina to see how that would impact the proliferation of progenitor cells in response in both organs. In these mice, inhibiting the Hippo pathway effectively caused supporting cells proliferation in the organ of Corti, an important step towards the regeneration of the ear’s sensory cells. In the retina, inhibiting the Hippo pathway induced the proliferation of progenitor cells known as Müller glia. Surprisingly, the researchers discovered that some of the Müller glia progeny, without further manipulation, converted to sensory photoreceptors and other neuronal cell types in the retina. A Window of Regenerative Opportunity “There have been reports that p27Kip1 levels drop following injury, so that might offer a brief window of opportunity for using a drug-like compound to inhibit the Hippo pathway and encourage regeneration in the ear and the eye,” said Gnedeva. “Alternatively, it could be possible to develop another drug-like compound to reduce p27Kip1 levels. So, our discoveries have identified potential new targets for stimulating the regeneration of both hearing and vision.” Reference: “The Hippo pathway and p27Kip1 cooperate to suppress mitotic regeneration in the organ of Corti and the retina” by Eva Jahanshir, Juan Llamas, Yeeun Kim, Kevin Biju, Sanyukta Oak and Ksenia Gnedeva, 3 April 2025, Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.2411313122 Additional co-authors are Yeeun Kim, Kevin Biju, and Sanyukta Oak from the Gnedeva Lab. This work was supported by federal funding from the National Institutes of Health’s National Institute on Deafness and Other Communication Disorders (grant 1R01DC020268, training grant T32DC009975, and clinician-scientist training grant 5R25DC019700). Disclosures Gnedeva is a co-inventor on three patent applications related to this work: 1. Lats kinase inhibitor to treat retinal degeneration (PCT application number PCT/US2024/023146; U.S. Patent and Trademark serial number usc0282prv); 2. Pyrrolopyridine-3- and 4-carboxamide compositions and methods for cellular proliferation (docket number 2877.035P1); and 3. Pyrrolo[2,3-b]pyridine-3-carboxamide compositions and methods for ameliorating hearing loss (application number 62970425). 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