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Avoid these four common mistakes.
With the arrival of autumn, people are increasingly engaging in outdoor activities, and accidents and injuries are becoming more common. When dealing with autumn injuries, many peo...
◆In 1962, Dr. Winter of the Royal Society of Medicine confimed in animal experiments that wound healing in Moisture conditions is twice as fast as in dry conditions.
◆In 1963, Hinman conducted human studies to confirm the scientificity of Moisture healing.
◆In August 2000, the U.S. Food and Drug Administration laid sρecial emphasis on maintaining a warm environment for wounds as a standard treatment method in the newly issued industry guidelines for wound medical supplies (external medicines and wound dressings).
These conclusions not only lay a foundation for the modern theory of Moisture wound treatment, but also ρromote the application of Moisture wound healing in care technology. A new wound care dressing, namely, the closed Moisture dressing, is produced.
1. Inappropriate local treatment of wounds: due to the lack of basic knowledge of the wound and improper Use of various dressings.
2. Humidity of wounds: cells, enzymes and growth factors on wounds do not function under dry conditions. When in a humid environment, its activity is enhanced, thus promoting wound healing.
3. Temperature of wounds: the activity of various cells and enzymes on wounds is the highest at normal body temperature. The research shows that if the temperature of wound surface is lower than body temperature more than 2℃, the activity of cells and enzymes decreases greatly.
4. Inadequate local blood supply to wounds: the increase of local pressure, friction, and shear force of local wound or inflammation of local small blood vessels leads to thrombosis, which is the decrease of blood supply in the local wound, thus affecting wound healing.
5. Infection of wounds: the infection of wounds can cause necrosis of local tissue cells and hinder wound healing.
6. Scab formation on the wounds: the formation of scab can affect the normal metabolism of wound and the migration of epithelial cells.
7. Pain of wounds: the pain of wounds will shrink the blood vessels around the wound, reduce the oxygen suρply of the tissue, and affect the reconstruction of the vascular tissue.
1. Obstruct microorganisms from entering wounds.
2. Keeρ the wound moisture and warm in the local environment state.
3. Promote the synthesis of various enzymes, activate the activity of growth factors and accelerate tissue healing.
4. Improve local micro-circulation and "awaken" self-cleaning ability of chronic wound.
5. In the Moisture enviroment, various cells (such as macrophages, neutrophils, etc.) in the wound are activated and phagocytose pathogenic microorganisms in the wound.
6. The increased concentrations of carbon dioxide in wounds, accelerate the formation of new blood vessels and granulation tissues.
7. The Moisture gel formed on the wound protects the new tissue, reduces the nerve endings stimulation and relieves pain.
8. Accelerate debridement and support the formation of granulation tissue and epidermis in the damaged part.
9. Reduce local pressure, friction and shear force, improve blood supply.
10. No scab healing, faster division of epithelial cells, and easy to migrate, and ultimately shorten the healing time.
Globally, colorectal cancer (CRC) is one of the most common cancers and a leading cause of cancer-related death. A groundbreaking study published in Gut recently revealed the role of lipid metabolism disorders in colorectal cancer and pointed to a possible therapeutic avenue that converts chronic inflammation into an opportunity to treat cancer. The study, led by researchers from the University of South Florida, USA, explored the mechanisms of persistent inflammation in colorectal cancer by integrating lipidomics, targeted molecules, and spatial transcriptomics, and proposed new therapeutic strategies to address these disorders. The study showed that arachidonic acid (AA)-derived lipid mediators (such as leukotrienes) associated with chronic inflammation were significantly upregulated in colorectal cancer tissues, while pro-resolution mediators (such as lipoxins) were almost absent. Background: The role of chronic inflammation in the progression of colorectal cancer has been highlighted, often attributed to an imbalance between pro-inflammatory and inflammatory resolution or pro-resolving processes. During normal wound healing, a process called lipid mediator class switching leads to a transition from inflammation to resolution, which also involves molecules such as lipoxins and resolvins. However, colorectal cancer appears to exhibit impaired class switching, resulting in persistent inflammation. The research team used a multimodal approach to examine lipid metabolism in colorectal cancer using 81 paired tumor and normal tissue samples. Untargeted lipidomics analysis focused on 40 paired samples, while targeted lipidomics assessed AA pathway-related mediators. Liquid chromatography tandem mass spectrometry (LC-MS/MS) was used for both untargeted and targeted lipidomics analysis. Results: Colorectal cancer tissues exhibited a distinct pro-inflammatory lipid profile compared with normal tissues. Quantitative lipidomic analysis revealed elevated levels of AA-derived mediators associated with the enzyme ALOX5, including leukotrienes and 5-hydroxyeicosatetraenoic acid (5-HETE). In contrast, pro-resolving mediators, such as lipoxins, were significantly deficient, suggesting a defect in lipid mediator class switching. In terms of therapeutic significance, the researchers proposed "dissipative medicine", emphasizing the therapeutic potential of specialized pro-dissipative mediators (SPMs) such as dissipatives and protectins in restoring lipid metabolic balance. Gene expression analysis also revealed overexpression of pro-inflammatory genes in colorectal cancer tissues, such as ALOX5, ALOX5 activation protein (ALOX5AP), and leukotriene-A4 hydrolase (LTA4H). These genes are closely associated with inflammatory biomarkers and macrophage markers, emphasizing the role of tumor-associated macrophages (TAMs) in maintaining inflammation. Lipidomic analysis revealed specific structural lipid changes, including enrichment of phospholipids containing linoleic acid and AA. These changes were also associated with chronic inflammation and tumor progression, suggesting metabolic disturbances in the tumor microenvironment. The researchers concluded that a distinct imbalance between pro-inflammatory and resolving mediators underlies the persistent inflammatory state in colorectal cancer. By identifying these key molecular and cellular mechanisms, the study provides insights into potential therapeutic strategies that could focus on restoring lipid class switching through endogenous or exogenous pro-resolving mediators. Journal reference: Soundararajan, R., Maurin, MM, Rodriguez-Silva, J., Upadhyay, G., Alden, AJ, Gowda, SB, Schell, MJ, Yang, M., Levine, NJ, Gowda, D., Sundaraswamy, PM, Hui, S., Pflieger, L., Wang, H., Marcet, J., Martinez, C., Bennett, RD, Chudzinski, A., Karachristos, A., & Nywening, TM (2024). Integration of lipidomics with targeted, single cell, and spatial transcriptomics defines an unresolved pro-inflammatory state in colon cancer.
Our solutions start with a need. Patients and healthcare professionals inspire us to design medical solutions for wound management, surgery and pressure ulcer prevention. We want to enhance performance at every point of care – from the operating room to the home.
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