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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]

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.

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]

Aims and objectives: To establish a simple score that enables nurses to quickly, conveniently and accurately identify patients whose condition may change during intrahospital transport. Background: Critically ill patients may experience various complications during intrahospital transport; therefore, it is important to predict their risk before they leave the emergency department. The existing scoring systems were not developed for this population. Design: A prospective cohort study. Methods: This study used convenience sampling and continuous enrolment from 1 January, 2019, to 30 June, 2021, and 584 critically ill patients were included. The collected data included vital signs and any condition change during transfer. The STROBE checklist was used. Results: The median age of the modelling group was 74 (62, 83) years; 93 (19.7%) patients were included in the changed group, and 379 (80.3%) were included in the stable group. The five independent model variables (respiration, pulse, oxygen saturation, systolic pressure and consciousness) were statistically significant (p <.05). The above model was simplified based on beta coefficient values, and each variable was assigned 1 point, for a total score of 0–5 points. The AUC of the simplified score in the modelling group was 0.724 (95% CI: 0.682–0.764); the AUC of the simplified score in the validation group (112 patients) was 0.657 (95% CI: 0.566–0.741). Conclusions: This study preliminarily established a simplified scoring system for the prediction of risk during intrahospital transport from the emergency department to the intensive care unit. It provides emergency nursing staff with a simple assessment tool to quickly, conveniently and accurately identify a patient's transport risk. Relevance to clinical practice: This study suggested the importance of strengthening the evaluation of the status of critical patients before intrahospital transport, and a simple score was formed to guide emergency department nurses in evaluating patients. [ABSTRACT FROM AUTHOR]

Ferroptosis is regulated by genes and participates in the physiological and pathological processes of ischemia-reperfusion injury, stroke, tumor and other diseases. The pathogenic mechanism is not yet clear. It is known that regulating p53 gene can induce ferroptosis of endothelial cells and tumor cells. Inhibiting ferroptosis enables GPX4 to function normally, blocking lipid oxidation on cell membranes, reducing the accumulation of reactive oxygen species (ROS), and protecting normal cells. In view of the polyreactivity of ferroptosis, it may help kill cancer cells and may damage normal cells. Therefore, genes related to regulatory ferroptosis sensitivity and the trigger mechanism need to be elucidated urgently. This article mainly reviews the known functional mechanisms of regulatory ferroptosis sensitive genes such as GPX4, FSP1, SLC7A11, P53, et al, in order to provide a reference for the in-depth analysis of ferroptosis research and the selection of drugs for major diseases. [ABSTRACT FROM AUTHOR]