Skin ulcers are a serious complication of diabetes. Diabetic patients suffer from vascular lesions and complications such as peripheral neuritis, peripheral vascular lesions, and collagen abnormalities, which result in skin wounds that are refractory and often develop into chronic ulcers. The healing of skin ulcers requires an inflammatory reaction, wound proliferation, remodeling regulation, and control of stem cells. Studies investigating diabetic cutaneous ulcers have focused on cellular and molecular levels. Diabetes can cause nerve and blood vessel damage, and persistent high blood sugar levels can cause systemic multisite nerve damage based on peripheral neuropathy. The long-term hyperglycemia state enables the polyol glucose metabolism pathway to be activated, increasing the accumulation of toxic substances in the vascular injured nerve tissue cells. Sustained hyperglycemia leads to dysfunction of epithelial cells, leading to a decrease in pro-angiogenic signaling and nitric oxide production. In addition, due to impaired leukocyte function in hyperglycemia, immune function is impaired and the immune response at relevant sites is insufficient, making diabetic foot more difficult to heal. The Wnt/β-catenin pathway is a highly conserved signal transduction pathway involved in a variety of biological processes, such as cell proliferation, apoptosis, and differentiation. It is considered an important pathway involved in the healing of skin wounds. This article summarizes the mechanism of action of the Wnt/β-catenin pathway involved in the inflammatory responses to diabetic ulcers, wound proliferation, wound remodeling, and stem cells. The interactions between the Wnt signal pathway and other metabolic pathways are also discussed.
Diabetic chronic cutaneous ulcers (DCU) are one of the serious complications of diabetes mellitus, occurring mainly in diabetic patients with peripheral neuropathy. Recent studies have indicated that microRNAs (miRNAs/miRs) and their target genes are essential regulators of cell physiology and pathology including biological processes that are involved in the regulation of diabetes and diabetes-related microvascular complications. in vivo and in vitro models have revealed that the expression of some miRNAs can be regulated in the inflammatory response, cell proliferation, and wound remodelling of DCU. Nevertheless, the potential application of miRNAs to clinical use is still limited. Here, we provide a contemporary overview of the miRNAs as well as their associated target genes and pathways (including Wnt/β-catenin, NF-κB, TGF-β/Smad, and PI3K/AKT/mTOR) related to DCU healing. We also summarize the current development of drugs for DCU treatment and discuss the therapeutic challenges of DCU treatment and its future research directions.
A general formula for plastic collapse load of elliptical heads under internal pressure is useful in plastic collapse design and integrity assessment of pressure vessels. Plastic collapse load of steel elliptical heads with different shapes and thickness was computed by finite element analysis using elastic-perfectly plastic constitutive model, and a formula with maximum relative error less than 6% was derived from the numerical results. The formula is a function of the yield strength of materials, the ratio of major axis Di to minor axis 2hi and that of outer diameter Do to inner diameter Di, and is applicable to steel elliptical heads with Di/2hi within 1–2.6 and Do/Di within 1.001–1.300.
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