Corrigendum to "Fumaria officinalis-loaded chitosan nanoparticles dispersed in an alginate hydrogel promote diabetic wounds healing by upregulating VEGF, TGF-ß, and b-FGF genes: A preclinical investigation".

[This corrects the article DOI: 10.1016/j.heliyon.2023.e17704.].

Fumaria officinalis-loaded chitosan nanoparticles dispersed in an alginate hydrogel promote diabetic wounds healing by upregulating VEGF, TGF-ß, and b-FGF genes: A preclinical investigation.

Diabetic wounds may become chronic if left untreated. In the current study, a potential wound dressing was developed by incorporating fumaria officinalis extract-loaded chitosan nanoparticles (FOE-CHNPs) into calcium alginate hydrogel. The produced hydrogel was evaluated regarding its microarchitecture, cytotoxicity, cell migration activity, cytoprotective potential, porosity, in vitro anti-inflammatory activity, and drug release profile. Then, the healing function of FOE-CHNPs/calcium alginate hydrogel was compared with a marketed wound care product in a rat model of diabetic wound. In vitro study showed that the hydrogel system promoted skin cells viability and migration. In vivo wound healing assay showed that the animals treated with the FOE-CHNPs/calcium alginate hydrogel had comparable wound healing potential with the GranuGEL® as the marketed wound care hydrogel. Gene expression studies showed that FOE-CHNPs/calcium alginate hydrogel upregulated the tissue expression levels of collagen type 1, collagen type 2, VEGF, b-FGF and TGF-B genes. This preclinical research, suggests potential use of FOE-loaded calcium alginate hydrogel system in treating diabetic wounds in the clinic.

Intraoperative salvaging of failure to harvest the bi-paddle anterolateral thigh flap: a case series.

Background: The size and versatility of anterolateral thigh (ALT) flap enables a bi-paddle flap to cover complex and extensive defects optimally. However, it is characterized by variations in the sources of blood vessels and in the number of perforators, which increases the chances of failure of harvesting a bi-paddle flap. We present our method to overcome such failure. This is the first study exploring the optimal salvaging algorithm to overcome harvesting failure with the bi-paddle ALT flap. Methods: From January 2014 to December 2020, in 9 patients to be treated with bi-paddle ALT flap for soft-tissue defects (range, 48-288 cm2), there was failure of flap harvest because of perforator variations. We redesigned and converted the flaps to other forms for harvest intraoperatively, based on the characteristics of the defect, and the number and sources of perforators. Results: Salvage of flap harvest was successfully performed in all 9 cases. In 4 cases the flap with a single perforator was converted to widened-single-perforator flaps; in 2 cases, a single perforator was converted to a de-epithelialized flap; in 2 cases of 2 perforators from different main branches, conversion was to sequential chimeric flaps; in the remaining case of 2 perforators from the descending branch and transverse branch, conversion was to a combined transverse-and-descending branches flap. Venous compromise occurred in only 1 case, and the patient survived after revised surgery. Local infection in the receiving area occurred in 3 cases, and was cured by wound dressing. All flaps survived (follow-up 5-24 months). Conclusions: Despite preoperative preparation, anatomic variations resulted in failure of bi-paddle ALT flap harvesting. As shown by our results, it is feasible to redesign and convert the bi-paddle flap to other forms based on the defect characteristics, and the number and sources of perforators.

Upregulation of miR-214 Induced Radioresistance of Osteosarcoma by Targeting PHLDA2 via PI3K/Akt Signaling.

Osteosarcoma is an aggressive bone tumor with high resistance to radiotherapy. Pleckstrin homology-like domain family A member 2 (PHLDA2) displays low expression in human osteosarcoma as a proapoptosis factor. miRNAs have been shown to be important in modulating translation and therapeutic responsiveness in solid tumors. Herein, we used luciferase assay to show that miR-214 downregulates the PHLDA2 expression by targeting its 3'-untranslated region (UTR). A high level of miR-214 was identified in tumor tissues from 30 osteosarcoma patients via qPCR analysis, associated positively with lung metastasis. Ectopic expression miR-214 enhanced radioresistance in osteosarcoma cells, with decreased IR-induced apoptosis. Moreover, the depletion of miR-214 enhanced radiosensitivity in both osteosarcoma cells and mouse xenograft models. Importantly, we showed that miR-214 regulated the activation of phosphatidylinositol-3-kinase/Akt signaling pathway by inhibiting PHLDA2. Finally, the introduction of PHLDA2 cDNA lacking the 3'-UTR or treatment with Akt inhibitor LY294002 partially abrogated miR-214-induced radioresistance. In summary, our results reveal that the upregulation of miR-214 as a frequent event in osteosarcoma contributes to radioresistance by regulating the PHLDA2/Akt pathway. The miR-214/PHLDA2/Akt axis provides a new avenue toward understanding the mechanism of radiosensitivity and may be a potential target for osteosarcoma intervention.