Hematoporphyrin photodynamic therapy for treatment of pathological scar with ulceration: A case report.

Pathological scars result from abnormal wound healing and represent a fibrotic process in the repair of skin injuries. Post-burn scars are prone to malignant transformation, especially when ulceration occurs, raising concerns for precancerous lesions. We report a case of a 56-year-old female with a 50-year history of a large burn scar on her left forearm. The scar developed non-healing ulceration with local pain and itching over the past three years. Treatment with hematoporphyrin photodynamic therapy (HpD-PDT) led to resolution of the ulceration, thinning of the scar tissue, and significant alleviation of pain and itching. After a five-year follow-up, there has been no recurrence of ulceration, suggesting that photodynamic therapy effectively promotes wound healing in scarred tissue with ulcerations.

Constructing heterogeneous single-cell landscape and identifying microenvironment molecular characteristics of primary and lymphatic metastatic head and neck squamous cell carcinoma.

BACKGROUND: Head and neck squamous cell carcinoma (HNSCC) accounts for more than half of head and neck tumors, roughly 90%. This study focused on constructing the heterogeneous landscape using single-cell and bulk transcriptomic data to identify molecular characteristics of the microenvironment in primary and lymphatic metastatic head and neck squamous carcinomas. METHOD: The study enrolled 23 HNSCC samples with scRNA-seq data and 546 HNSCC samples from TCGA. We used Monocle to sort the cells and used CellPhoneDB to explore the cell-cell interactions. Infercnv, which was used to infer cells with apparent copy number variation based on single-cell sequencing transcriptome data. We re-evaluated HNSCC bulk RNA transcriptome data to characterize the functions of different cell types in shaping the immune microenvironment of HNSCC. RESULTS: We combined genealogical reconstruction, CNV inference, and cellular interactions to uncover the characteristics of distinct cell populations in different disease states, differences in cancer and immune cell lineages of differentiation trajectories, and interactions between non-immune and immune cell. PD-1 and PD-L1/PD-L2 expressed extremely rare in T cells, the immune checkpoint molecule KLRB1-CLEC2D achieved a high-level expression. We identified three microenvironment-based HNSCC subtypes associated with the prognosis of HNSCC patients. CONCLUSIONS: In summary, the present study dissected the intratumoral heterogeneity and immune microenvironment of primary and metastatic HNSCC, which is crucial to reveal the mechanisms of resistance to immunotherapy in HNSCC in different disease states and is expected to assist in the further investigation of the mechanism of HNSCC cell metastasis and guide the treatment of clinical patients.

Up-regulation of caveolin 1 mediated by chitosan activates Wnt/ ß-catenin pathway in chronic refractory wound diabetic rat model.

Diabetes mellitus (DM) can be implicated in the perturbations of vascular integrity and the dysfunction of angiogenesis. Chitosan has the advantage of promoting the vascular endothelial cell proliferation. However, the molecular mechanism of action in the promotion of wound healing by chitosan derivatives is still debated. In the current study, DM with chronic wound (CW) model rats were prepared and treated with chitosan. Vascular endothelial cells isolated from granulation tissues were conducted by RNA sequencing. Two thousand three hundred and sixteen genes were up-regulated, while 1,864 genes were down-regulated after chitosan treatment compared to CW group. Here, we observed that caveolin 1 (CAV1) was highly expressed induced by chitosan. Furthermore, we observed that CAV1 knockdown could compromise the activation of Wnt pathway by reduction of ß-catenin in rat aortic endothelial cells (RAOECs) and brain endothelium four cells (RBE4s). Moreover, we determined a direct interaction between CAV1 and ß-catenin by IP assay. The C-terminus of CAV1 and ß-catenin (24 to 586 amino acids) contributed to the interaction of these two proteins. Finally, the protein docking analysis indicated that the fragments of ß-catenin (253-261 'FYAITTLHN' and 292-303 'KFLAITTDCLQI') might have affected the structure by CAV1 and facilitated the resistance to degradation. Taken together, our study demonstrates that chitosan can up-regulate CAV1 expression, and CAV1 can interact with ß-catenin for promotion of canonical Wnt signaling pathway activity. Our results deepens the molecular mechanism of the Wnt pathway in vascular endothelial cells and is beneficial to developing new targets to assist in enhancing the pharmacological effect of chitosan on wound healing and angiogenesis against DM.