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Marjolin's ulcer is described as malignant lesions developed in the injured skin, which can cause several kinds of malignancies. Our results showed that no HER2 but p53 was detected in Majorlin's ulcer samples. Meanwhile, by statistical analysis, we found that the positive rate of p53 in Majorlin's ulcer samples was associated with the pathological type of ulcer canceration and degree of tumor differentiation. The positive expression rate of vascular endothelial growth factor (VEGF) was 62.5% in poorly differentiated squamous cell carcinoma (SCC), 39.4% in moderately differentiated SCC, and 66.7% in well-differentiated SCC, respectively. Furthermore, some cases of Majorlin's ulcer with positive P53 were negative for VEGF, while some cases with positive VEGF were negative for P53. Image superposition showed that VEGF expression was absent or minimal in p53-positive cases. However, P53 was not expressed or rarely expressed in VEGF-positive cases. Our results of this study will suggest that P53 can be used as the mark of Marjolin's ulcer differentiation, and there may be some interaction between P53 and VEGF in Marjolin's ulcer. The regulation of microenvironment in the oncogenesis, progression, and differentiation of Marjolin's ulcer is complex and needs further study., (© The Author(s) 2023. Published by Oxford University Press on behalf of the American Burn Association. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

The objective of this study was to evaluate the predictive role of CD21 low B cells as markers of new digital ulcers in systemic sclerosis patients. Peripheral blood B cell subpopulations and clinical assessments have been evaluated in 74 systemic sclerosis patients at baseline and after a 12-month follow-up. After a 12-month follow-up, 23 (31.1%) systemic sclerosis patients developed new digital ulcers. The median percentage of CD21 low B cells was significantly higher in patients with than without new digital ulcers [10.1 (4.3-13.6) versus 4.8 (3.5-7.4); p < 0.01]. The 10% cut-off shows good diagnostic accuracy [area under the curve (AUC) = 0.732, confidence interval (CI) = 0.587-0.878; P = 0.01]. Kaplan-Meier curves show a significantly reduced free survival from new digital ulcers in systemic sclerosis patients with CD21 low B cells ≥ 10% (p < 0.0001). In multivariate analysis, CD21 low B cells ≥ 10%, modified Rodnan skin score (mRSS) and systolic pulmonary arterial pressure (sPAP) are associated with the development of new digital ulcers. We hypothesize that CD21 low B cells are a predictive marker of new digital ulcers in systemic sclerosis patients., (© 2021 The Authors. Clinical & Experimental Immunology published by John Wiley & Sons Ltd on behalf of British Society for Immunology.)

Background: Regulated alteration of connexin expression has been shown to be integral to acute wound repair. Downregulation of the gap-junction protein connexin 43 at the wound edge has been correlated with keratinocyte and fibroblast migration, while abnormal overexpression of connexin 43 significantly perturbs healing, as shown in the streptozotocin diabetic rodent impaired healing model., Objectives: To examine the protein expression levels of connexin 43, in addition to connexins 26 and 30, in a variety of human chronic wounds., Methods: Wound-edge punch biopsies and a matched control from the arm were taken from a cohort of patients with venous leg, diabetic foot or pressure ulcers. Wound connexin expression in each patient was compared with that in a matched, nonwounded arm punch. Tissue was sectioned, stained and imaged by confocal microscopy using identical parameters per patient to permit quantification., Results: Epidermal connexin 43, connexin 26 and connexin 30, and dermal connexin 43 were discovered to be strikingly upregulated in every ulcer from all three wound types, pointing to connexin upregulation as a common feature between chronic wounds., Conclusions: This result supports efforts to target connexin 43 to promote cell migration and wound healing in chronic ulcers., (© 2015 British Association of Dermatologists.)

Stage-specific embryonic antigen-3 (SSEA-3)-positive multipotent mesenchymal cells (multilineage differentiating stress-enduring [Muse] cells) were isolated from cultured human adipose tissue-derived stem/stromal cells (hASCs) and characterized, and their therapeutic potential for treating diabetic skin ulcers was evaluated. Cultured hASCs were separated using magnetic-activated cell sorting into positive and negative fractions, a SSEA-3+ cell-enriched fraction (Muse-rich) and the remaining fraction (Muse-poor). Muse-rich hASCs showed upregulated and downregulated pluripotency and cell proliferation genes, respectively, compared with Muse-poor hASCs. These cells also released higher amounts of certain growth factors, particularly under hypoxic conditions, compared with Muse-poor cells. Skin ulcers were generated in severe combined immunodeficiency (SCID) mice with type 1 diabetes, which showed delayed wound healing compared with nondiabetic SCID mice. Treatment with Muse-rich cells significantly accelerated wound healing compared with treatment with Muse-poor cells. Transplanted cells were integrated into the regenerated dermis as vascular endothelial cells and other cells. However, they were not detected in the surrounding intact regions. Thus, the selected population of ASCs has greater therapeutic effects to accelerate impaired wound healing associated with type 1 diabetes. These cells can be achieved in large amounts with minimal morbidity and could be a practical tool for a variety of stem cell-depleted or ischemic conditions of various organs and tissues., (©AlphaMed Press.)

Despite the heterogeneity of SSc, almost all patients have skin involvement. As such, skin manifestations are critical in the initial diagnosis of SSc and in the subsequent sub-classification into the different subsets of disease. The two principal subsets are lcSSc and dcSSc. The main difference between these two subsets is the speed of disease progression and the extent and severity of skin and visceral involvement; lcSSc has an insidious onset with skin involvement confined largely to the face and extremities. Whilst vascular manifestations of SSc such as pulmonary arterial hypertension are typically more common in lcSSc, patients in both subsets can develop ischaemic digital ulcers. In dcSSc, disease progression is very rapid, with skin thickening extending beyond the extremities and earlier, more widespread internal organ involvement. DcSSc is generally considered to be the more severe subset of the disease. Skin scores in SSc correlate inversely with survival and are considered a valuable marker of disease severity. Skin involvement is easily detectable and, using the modified Rodnan skin score, the degree of skin fibrosis can be quantified. As well as general management measures, a number of targeted therapies are commonly used for treatment of cutaneous manifestations of SSc. These include the intravenous prostanoid iloprost and the dual endothelin receptor antagonist bosentan, which is approved in Europe for the prevention of new digital ulcers.

Carcinoembryonic antigen (CEA) is recognized as being important not only as a tumour marker, but also as a cell adhesion molecule in the metastasis of malignant tumour cells, and in the development of inflammatory disorders in some organs. However, the role played by this antigen in inflammatory dermatoses has not been studied previously. To investigate the expression of CEA in inflamed skin, we performed immunohistochemical studies to detect the antigen in both frozen and formalin-fixed, paraffin-embedded biopsy specimens of inflammatory dermatoses, using five different monoclonal antibodies and one polyclonal antibody against human CEA or CEA-related molecules. CEA and CEA-related antigens were expressed by epidermal keratinocytes and by some infiltrating inflammatory cells in inflamed skin. The expression was observed primarily in the upper part of the malpighian layers of the epidermis. On the basis of the distribution of this expression, we suggest an additional role for CEA-related molecules, differing from their roles as tumour markers and adhesion molecules, namely that these molecules may be associated with the state of differentiation of epidermal keratinocytes. Unexpected expression of CEA-related antigens was seen on normal follicular keratinocytes. Thus, it is conceivable that CEA-related antigen may also play a role in the biology of hair follicles.

In congenital deficiency of leucocyte-adherence glycoproteins (CDLG) there is an immunodeficiency with impaired leucocyte function and cutaneous and extracutaneous infections occur. In more than 30% of cases the condition has a fatal course. We report the skin manifestations of three siblings with CDLG in which areas of skin necrosis occurred that resembled pyoderma gangrenosum.

Non-enzymatic glycosylation of keratin from the stratum corneum of the sole of the foot was measured by the thiobarbituric acid technique in thirty diabetic and thirty control subjects. A significant increase in the level of glycosylation was demonstrated in the diabetic subjects (P less than 0.001). HbA1 levels were measured in a further eighteen subjects at the same time as keratin was removed, and in this group a significant association between non-enzymatic glycosylation of that protein and diabetic control was demonstrated (P less than 0.01). In vitro incubation of keratin in the presence of free glucose produced increased non-enzymatic glycosylation (P less than 0.01) and this effect was blocked by incubation in the presence of increasing concentrations of aspirin (P less than 0.01). Measurement of non-enzymatic glycosylation of keratin in a further group of twenty diabetics with neuropathic ulceration showed a significant increase in levels when compared with a group of diabetics without ulcers (P less than 0.05). As keratin is the principle structural protein of the stratum corneum of the sole of the foot, it is possible that changes in this protein associated with non-enzymatic glycosylation may contribute to abnormalities seen in the skin of the feet of diabetics.