Psoriasis is a multisystem disease affecting about 2% of the population, while keratin16 (KRT16) has been reported to participate in psoriasis. However, the specific mechanism of KRT16 in psoriasis was inadequately investigated. The objective of the study was to elucidate the mechanism by which siRNA‐mediated silencing of KRT16 affects keratinocyte proliferation and vascular endothelial growth factor (VEGF) secretion in psoriasis through the extracellular signal‐related kinase (ERK) signaling pathway. Psoriasis‐related core gene KRT16 was screened out. Then, the expression of KRT16, VEGF, and ERK signaling pathway‐related genes was detected in psoriatic patients. To further investigate the mechanism of KRT16, keratinocytes in psoriatic patients were treated with KRT16 siRNA or/and ERK inhibitor (PD98059) to detect the changes in related gene expression and cell survival. KRT16 was involved in psoriasis development. The expression levels of KRT16, p‐ERK1/2, and VEGF in lesion tissues are significantly elevated. Keratinocytes treated with KRT16‐siRNA and KRT16‐siRNA + PD98059 exhibited reduced KRT16, p‐ERK1/2, and VEGF expression. The cell survival rate in cells treated with KRT16‐siRNA, PD98059, and KRT16‐siRNA + PD98059 reduced significantly. These findings indicate that silencing KRT16 inhibits keratinocyte proliferation and VEGF secretion in psoriasis via inhibition of ERK signaling pathway, which provides a basic theory in the treatment of psoriasis.
Background The aim of this study was to evaluate the effectiveness and safety of remifentanil-based fast-track anesthesia for intraoperative device closure of atrial septal defects (ASDs). Material/Methods The clinical data of 152 pediatric patients who received intraoperative device closure of ASD in our hospital from January 2015 to December 2017 were retrospectively analyzed. Patients were divided into 2 groups: group F (remifentanil-based fast-track anesthesia group, n=72) and group C (fentanyl-based routine anesthesia group, n=80). The relevant data from 2 groups were collected and analyzed. Results No significant differences were found in the preoperative data or intraoperative hemodynamic index between these 2 groups. Group C was significantly inferior to group F regarding the duration of mechanical ventilation, length of intensive care unit (ICU) stay, length of hospital stay, and hospitalization expenses (P<0.05). In terms of postoperative complications, no death, third-degree atrioventricular block, occluder detachment, or residual leakage was reported in either group. The incidence of lung infections and bronchospasm was significantly higher in group C than in group F. There were no anesthetic-related complications. Conclusions The application of remifentanil-based fast-track anesthesia for intraoperative device closure of ASD is as effective and safe as fentanyl-based routine anesthesia. Moreover, remifentanil-based fast-track anesthesia has the advantages of shorter duration of mechanical ventilation, shorter length of hospital and ICU stay, fewer postoperative complications, and lower hospitalization expenses, and is therefore worthy of promotion in clinical practice.
Background: To further the exploration of the pathogenesis of mild cognitive impairment (MCI), we aimed to determine the appropriate dose for a rapidly established MCI rat model using D-galactose (D-gal), with lasting cognitive effects. Methods:In Experiment 1, we evaluated various D-gal concentrations (100-2,000 mg/kg/day), and determined that, compared with saline injections of the same volume. In Experiment 2, we evaluated the duration of the effect of 1,000 mg/kg/day D-gal injections for 1 week, with MWM testing initiated at 1 day, 1 month, and 3 months after completion of the injection regime in three model groups, respectively. Results:In Experiment 1, D-gal injections at a concentration of 1,000 mg/kg/day for 1 week was adequate to induce a significantly worse Morris water maze (MWM) test performance and pathomorphologic changes in the hippocampus, with MWM testing initiated 1 day after completion of the injection regime. In Experiment 2, Before modeling, the overall condition (fur, mental state, foraging behavior, and activity level), body weight, swimming speed, and swimming time did not significantly differ between the control (saline injections) and model groups (D-gal injections). After modeling, MWM test performance was considerably worse (longer escape latencies and fewer platform crossings within 90 seconds) in the model groups than in the control group, without significant differences among model groups. Furthermore, movement trajectories were similar among model groups.Conclusions: These results demonstrate that subcutaneous injections of D-gal 1,000 mg/kg/day for 1 week produce changes consistent with the characteristics and pathological processes of MCI. Thus, highdose D-gal injection allows the rapid establishment of an MCI model that is effective and sustainable.
Background: This study aimed to investigate the preventive effect of translocator protein 18kDa (TSPO) ligand PK11195 on amnestic mild cognitive impairment (aMCI), as well as its influence on astrocytes, in order to identify effective ways to prevent aMCI.Methods: Male SD rats were randomly divided into control group (n=10), aMCI group (n=10), PK11195 group (n=10), PK11195 + D-gal group (n=10). The preventive effect of PK11195 on aMCI in rats was evaluated. The cognitive function of rats in four different treatment groups was determined using the Morris water maze (MWM), as well as whole-brain pathology and immunofluorescence of rat brain tissue. Results:The results of the MWM behavioral test showed that rats pre-treated with PK11195 had improved escape latency and a higher number of platform crossings compared with the aMCI model rats.PK11195 was also shown to prevent the D-galactose (D-gal)-induced senescence of pyramidal cells in the hippocampal CA1 region and to inhibit the apoptosis of astrocytes. At the same time, compared with the aMCI model rats, the TSPO in the brain tissue of rats pretreated with PK11195 had a lower distribution density.Conclusions: Our results prove that PK11195 can effectively prevent D-gal-induced decline of learning and memory function as well as inhibit abnormal changes of related cells.
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