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The aim of this study was to reveal the photobleaching characteristics of α-(8-quinolinoxy) zinc phthalocyanine (ZnPc-F7), a new type of amphiphilic complex. Normal saline (NS), pure Roswell Park Memorial Institute (RPMI)-1640 medium (1640), RPMI-1640 medium containing 10% fetal calf serum, and cell suspension were used as solvents to study the photobleaching of ZnPc-F7 in different solutions. Absorbance and fluorescence spectra were measured. Photobleaching kinetics were observed after irradiation for 3–180 min with ZnPc-F7 concentrations of 1–40.00μg/mL. An in vivo imaging system was used to observe the distribution and photobleaching of ZnPc-F7 in mice. ZnPc-F7 was bleached both in vitro and in vivo after exposure to laser energy at 670 nm. ZnPc-F7 was not bleached without irradiation. ‘The type of solvent, irradiation time, and initial concentration influenced the photobleaching rate. Rapid initial phases followed by a slower rate of photobleaching were observed in all four solutions. Fluorescence of ZnPc-F7 in mouse skin was steady and then increased 24 h after injection. There was no significant difference in the extent of fluorescence between normal and psoriasis-like mice. Local administration of ZnPc-F7 showed higher fluorescence intensity in skin at an early time than intravenous injection and lower content in organs after 24 h.

Pulmonary arterial hypertension (PAH) is a malignant cardiovascular disease. Eukaryotic initiation factor 2α (eIF2α) plays an important role in the proliferation of pulmonary artery smooth muscle cells (PASMCs) in hypoxia-induced pulmonary hypertension (HPH) rats. However, the regulatory mechanism of eIF2α remains poorly understood in PAH rats. Here, we discover eIF2α is markedly upregulated in monocrotaline (MCT)-induced PAH rats, eIF2α can be upregulated by mRNA methylation, and upregulated eIF2α can promote PASMC proliferation in MCT-PAH rats. GSK2606414, eIF2α inhibitor, can downregulate the expression of eIF2α and alleviate PASMC proliferation in MCT-PAH rats. And we further discover the mRNA of eIF2α has a common sequence with N 6-methyladenosine (m6A) modification by bioinformatics analysis, and the expression of METTL3, WTAP, and YTHDF1 is upregulated in MCT-PAH rats. These findings suggest a potentially novel mechanism by which eIF2α is upregulated by m6A modification in MCT-PAH rats, which is involved in the pathogenesis of PAH. [ABSTRACT FROM AUTHOR]

The purpose of this study is to determine the impact of maggot debridement therapy (MDT) on macrophages during the healing process of diabetic foot ulcers (DFU). The activation phenotype of macrophages during wound healing following MDT was evaluated using double staining immunohistochemistry (IHC). In addition, markers associated with macrophage activation were discovered using immunoblotting and real‐time polymerase chain reaction (PCR). During the process of diabetic wound healing following MDT, the presence and over‐expression of M2 macrophages were observed, while the under‐expression of M1 macrophages was noted. In addition, the activation markers of macrophages exhibited a correlation with the indicated Th1/Th2 cytokines. MDT interventions have the potential to modulate macrophage activity, thereby aiding in the healing of diabetic foot wounds. [ABSTRACT FROM AUTHOR]

Background of the Study Diabetic foot ulcers (DFUs) are severe effect of diabetes. This research aimed to discover the role of micro‐ribonucleic acid (miRNA) in treating DFUs involved in maggot debridement therapy (MDT) via a miRNA chip study. A miRNA chip approach was adopted. Patients with diabetes (type 1 or 2) who had at least one‐foot ulcer (current or previous) were enrolled in the study. The alterations of miRNA expressions in the granulation tissue during treatment with MDT were measured. Following MDT, the increased expression of miR17‐92 was verified in vivo. The miR‐17‐3p expression increased, and Flk‐1 (vascular endothelial growth factor) expression was significantly reduced in patients with DFUs who received MDT (P < 0.01). Results from human umbilical vein endothelial cells that excrete or secrete showed consistency with in vitro findings (P < 0.001, P < 0.05). The overexpression of miR‐17‐3p demonstrated inhibitory activity on tube formation (P < 0.05). When DFUs were treated with MDT, it revealed that miR‐17‐3p had a negative regulatory effect on Flk‐1. [ABSTRACT FROM AUTHOR]