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ponent F had the potential to be used as natural anti-cancer agents.

Few studies have investigated the generation of induced pluripotent stem cells (iPSCs) derived from human primary chorionic villi (CV) cells. The present study aimed to explore an optimal electroporation (EP) condition for generating non-integrated iPSCs from CV cells (CV-iPSCs).

The EGFP plasmid was transfected into CV cells under different EP conditions to evaluate cell adherence and the rate of EGFP positive cells. Subsequently, CV cells were transfected with the pEP4-E02S-ET2K and pCEP4-miR-302-367 plasmids under optimal EP conditions. Finally, CV-iPSC pluripotency, karyotype analysis, and differentiation ability were investigated.

Following EP for 48h under different conditions, different confluency, and transfection efficiency were observed in CV cells. Higher cell density was observed in CV cells exposed to 200V for 100s, while higher transfection efficiency was obtained in cells electroporated at a pulse of 300V for 300s. To generate typical primitive iPSCs, CV cells were transfected with pEP4-E02S-ET2K and pCEP4-miR-302-367 plasmids using EP and were then cultured in induction medium for 20days under selected conditions. Subsequently, monoclonal iPSCs were isolated and were evaluated pluripotency with AP positive staining, the expression of OCT4, SOX2, and NANOG in vitro and the formation of three germ layer teratomas in vivo.

CV-iPSCs were successfully established under the conditions of 100μl shock cup and EP pulse of 200V for 300s for two times. This may provide a novel strategy for investigating the pathogenesis of several diseases and gene therapy.

CV-iPSCs were successfully established under the conditions of 100 μl shock cup and EP pulse of 200 V for 300 s for two times. This may provide a novel strategy for investigating the pathogenesis of several diseases and gene therapy.Network pharmacology is a bioinformatics-based research strategy aimed at identifying drug actions and facilitating drug discovery. click here In this study, network pharmacology was used for exploring the anti-epileptic multi-target mechanism of Rhizoma Coptidis. The possible protein targets of Rhizoma Coptidis were predicted by constructing the pathway and network of drug targets. Then, the interaction of the main active components of Rhizoma Coptidis and predicted candidate targets were verified using molecular docking technology. Finally, nine active compounds were selected from Rhizoma Coptidis. A total of 68 targets associated with Rhizoma Coptidis treating epilepsy. The key targets were AKT1, IL6, VEGFA, and TP53. According to GO functional enrichment analysis, 289 items of biological process, 33 items of cellular component, and 55 items of molecular function were obtained. A total of 89 signaling pathways were identified through KEGG pathway enrichment analysis (P less then 0.05), and HIF-1, TNF, and T-cell receptor signaling pathways were mainly related to epilepsy. Molecular docking showed quercetin and (R)-canadine combined well with the key targets. The active ingredient in Rhizoma Coptidis can regulate various signaling pathways, and have therapeutic effects on epilepsy.

Inactivated vaccines against coronavirus disease-2019 (COVID-19) offer an effective public health intervention to mitigate this devastating pandemic. However, little is known about their safety in patients with wheat-dependent exercise-induced anaphylaxis (WDEIA).

We recruited 72 WDEIA patients and 730 healthy matched controls who received an inactivated COVID-19 vaccine. Participants were monitored for 4 weeks after each immunization for adverse reactions and completed questionnaires regarding local and systemic reactions at 7 and 28 days after each vaccination. For those who had received the COVID-19 vaccine prior to enrollment, adverse event data were obtained retrospectively.

Local and systemic adverse events occurred at similar rates in the WDEIA group and the control group. In both groups, injection-site pain and fatigue were the most common local and systemic reactions, respectively. Compared with healthy controls, more allergic events were reported in the WDEIA group (after dose 1, 0.5% vs. 4.2%, p=0.019; after dose 2, 0% vs. 1.4%, p=0.089). Allergic reactions mainly manifested as rash, urticaria, and edema, which were mild and controllable. No serious allergic events were reported.

The adverse event profile of inactivated COVID-19 vaccine did not differ between WDEIA patients and healthy controls. The risk of allergic reactions in patients with WDEIA seems higher, but no anaphylaxis was reported, and the allergic reactions were controllable. Inactivated COVID-19 vaccines appear to be well-tolerated in WDEIA patients, but patients with potential allergy risks should be cautious.

The adverse event profile of inactivated COVID-19 vaccine did not differ between WDEIA patients and healthy controls. The risk of allergic reactions in patients with WDEIA seems higher, but no anaphylaxis was reported, and the allergic reactions were controllable. Inactivated COVID-19 vaccines appear to be well-tolerated in WDEIA patients, but patients with potential allergy risks should be cautious.

No studies are comparing the impact of the add-on leukotriene-receptor antagonist (LTRA) with a step-up dose of inhaled corticosteroids (ICS) in partly controlled asthma patients with asthma control test (ACT) score ˂ 23.

To study the effect of LTRA add-on therapy in comparison to a step-up to medium dose of ICS in partially controlled asthma.

An open-labeled randomized controlled trial was conducted in asthma subjects with partly controlled asthma who had been in regular receipt of low dose ICS. All subjects were assessed for asthma using ACT, daytime and nighttime symptoms, rate of relievers used, spirometry, and impulse oscillometry (IOS) at 3 and 6 months. Subjects were randomized to receive daily oral LTRA 10 mg or step-up medium dose of ICS.

Between June 2020 and January 2021, 50 participants were enrolled, all patients completing the study. After treatment, mean ACT scores were increased to more than 23 indicating well-controlled asthma in both groups, control being sustained throughout the whole 6-month study period (P ˂ 0.001). Within each group, ACT scores were improved by a minimal clinical important difference (MCID) ≥ 3 points at 6 months, compared to baseline values. There were significant decreases in nighttime and daytime symptoms, and the numbers of rescue relievers used in 4 weeks in both groups compared to baseline (P ˂ 0.001).

LTRA add-on therapy in partially controlled asthma patients is comparable with step-up to medium dose of ICS/LABA as regards asthma control.

LTRA add-on therapy in partially controlled asthma patients is comparable with step-up to medium dose of ICS/LABA as regards asthma control.

Protein tyrosine phosphatase receptor type O (PTPRO) belongs to the PTP (protein tyrosine phosphatase) family and is widely expressed in parenchymal cells, such as breast and lung epithelial cells. PTPRO has been shown to enhance inflammatory responses and has been implicated in the pathogenesis of inflammation-associated diseases. The role of PTPRO in pneumonia was investigated.

Human embryonic lung fibroblasts (HFL1) were treated with increasing concentrations of lipopolysaccharide at 5, 10, or 20 μg/mL to induce inflammatory and apoptotic injuries. Expression of PTPRO was detected by western blot. Inflammation and apoptosis were assessed by ELISA and flow cytometry assays, respectively.

Lipopolysaccharide induced decreased cell viability, and increased inflammation and apoptosis in HFL1. PTPRO was upregulated in HFL1 post lipopolysaccharide treatment, and silencing of PTPRO enhanced lipopolysaccharide-induced cell viability of HFL1, and suppressed the inflammation and apoptosis. However, overexpression of PTPRO aggravated lipopolysaccharide-induced cytotoxicity in HFL1. Overexpression of PTPRO upregulated protein expression of TLR4 and p-p65 in lipopolysaccharide-induced HFL1, while knockdown of PTPRO reduced the level of p-IκBα to downregulate levels of TLR4 and p-p65.

PTPRO contributed to pro-inflammatory and pro-apoptotic effects on lipopolysaccharide-induced HFL1 through activation of TLR4/NF-κB signaling.

PTPRO contributed to pro-inflammatory and pro-apoptotic effects on lipopolysaccharide-induced HFL1 through activation of TLR4/NF-κB signaling.

Pneumonia is a continuous and widespread disease with higher incidence, the effects of it on human life can be fearful. Tricin has been demonstrated to take part in the progression and development of diseases. However, the function of Tricin and its related regulatory pathways remain unclear. This study was planned to investigate the effects of Tricin on severe pneumonia.

The cell viability was detected through CCK-8 assay. The TNF-α, IL-1β and IL-6 levels were assessed through ELISA and RT-qPCR. The levels of MDA, SOD and GSH were tested through corresponding commercial kits. The protein expressions were examined through western blot.

In our study, the lipopolysaccharide (LPS) was firstly used to stimulate cell model for severe pneumonia. We discovered that Tricin had no toxic effects on BEAS-2B cells and the decreased cell viability induced by LPS was relieved by a dose-dependent Tricin treatment. Additionally, through ELISA and RT-qPCR, it was uncovered that Tricin reduced the LPS-induced inflammation through regulating TNF-α, IL-1β and IL-6. Furthermore, Tricin relieved LPS-induced oxidative stress through reducing MDA level and enhancing SOD and GSH levels. Finally, it was demonstrated that Tricin retarded LPS-activated AKT and MAPK pathways.

Our findings revealed that Tricin attenuated the progression of LPS induced severe pneumonia through modulating AKT and MAPK signaling pathways. This discovery might afford one novel sight for the treatment of severe pneumonia.

Our findings revealed that Tricin attenuated the progression of LPS induced severe pneumonia through modulating AKT and MAPK signaling pathways. This discovery might afford one novel sight for the treatment of severe pneumonia.

Although early diagnosis, antibiotic therapies, corticosteroid application, and health care services are conventional managements for pneumonia, antibiotic resistance and adverse reactions remain as limitations for pneumonia treatment.

The study attempted to evaluate the potential role of EPSTI1 against pneumonia and reveal its underlying mechanism.

Lipopolysaccharide (LPS) (5, 10, and 20 μg/mL) was applied in WI-38 cells to establish the

pneumonia model. Knockdown of epithelial-stromal interaction 1 (EPSTI1) was performed by transfection with EPSTI1 siRNA (siEPSTI1) into LPS-treated cells. Cell Counting Kit-8 assays were implemented to measure cell viability, and apoptotic cells were detected using flow cytometry. Interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) were quantified using enzyme-linked immunosorbent assay (ELISA). Immunoblotting and quantitative real-time polymerase chain reaction (qRT-PCR) were conducted to quantify EPSTI1 expression, and proteins related to nuclear factor κ-light-chain-enhancer of activated B cell (NF-κB) signaling, including p-p65, p65, p-IκBα, and IκBα.

EPSTI1 was highly expressed in LPS-treated WI-38 cells. Cell apoptosis was promoted, and cell viability was inhibited after being exposed to LPS. Besides, IL-1β, IL-6, and TNF-α were dramatically upregulated. Knockdown of EPSTI1 restored cell viability, inhibited cell apoptosis, and attenuated expressions of proinflammatory factors. Additionally, knockdown of EPSTI1 visibly decreased the increased ratios of p-p65/p65 and p-IκBα/IκBα induced by LPS. Knockdown of EPSTI1 alleviated inflammatory injury through the inactivation of the NF-κB pathway.

These results provided promising management in preventing pneumonia in patients.

These results provided promising management in preventing pneumonia in patients.