Umbilical cord blood mesenchymal stem cells (UC-BSCs) are cells with low immunogenicity and differentiation potential, and the transfer of exosomes carried by UC-BSCs can regulate innate and adaptive immunity and affect immune homeostasis. This is an area of focus for autoimmune illnesses such as systemic lupus erythematosus (SLE). The target of this research was to investigate the immunomodulatory effect of exosomes produced from mesenchymal stem cells on SLE and its mechanism. After isolation of peripheral blood mononuclear cells (PBMC) from the SLE group and healthy group and treatment of SLE-derived PBMCs with UC-BSC-derived exosomes, the mRNA levels of corresponding factors in cells under different treatments were determined by RT-PCR, Th17/Treg content was analyzed by FCM (flow cytometry), and the targeted binding of microRNA-19b (miR-19b) to KLF13 was identified by in vitro experiments and bioinformatics analysis. The findings demonstrated that PBMC cells from SLE patients had higher proportions of Th17 subsets than the control group, whereas Treg subgroups with lower percentages were discovered. miR-19b’s expression level was markedly reduced, which was inversely associated to the concentration of KLF13. In vitro experiments show that UC-BSC-derived exosome treatment can target KLF13 expression by increasing the miR-19b level, thereby regulating Th17/Treg balance and inhibiting the expression of inflammatory factors. According to the study’s findings, SLE patients have dysregulated expression of the genes miR-19b and KLF13, and UC-BSC exosomes could regulate Th17/Treg cell balance and inflammatory factor expression in SLE patients through miR-19b/KLF13.

The purpose of this study is to study the effect of curcumin derivative WZ10 on the proliferation, invasion and apoptosis of ovarian cancer OVCAR3 cells, and to explore its mechanism. MTT assay was used to detect the effect of WZ10 on the proliferation of ovarian cancer OVCAR3 cells; Annexin V/PI double staining flow cytometry was used to detect the effect of WZ10 on cell apoptosis; Transwell method was used to detect the effect of WZ10 on cell invasiveness; Western blot was used to investigate the effect of WZ10 Mechanisms affecting OVCAR3 activity in ovarian cancer in vitro. Our results show that WZ10 treatment could significantly inhibit the proliferation and invasion of OVCAR3 cells, induce apoptosis of OVCAR3 cells in a dose-dependent manner. After knockdown of Hippo expression with sh-RNA, further combined treatment with WZ10 had no significant image on ovarian cancer OVCAR3 cells. In conclusion: WZ10 can significantly inhibit the proliferation of OVCAR3 cells, reduce cell invasion and proliferation by downregulating the activation of Hippo-YAP pathway, and induce cell apoptosis.

The air kerma is a key parameter in medical diagnostic radiology. Radiologists use the air kerma parameter to evaluate organ doses and any associated patient hazards. The air kerma can be simply described as the deposited kinetic energy once a photon passes through the air, and it represents the intensity of the radiation beam. Due to the heel effect in the X-ray sources of medical imaging systems, the air kerma is not uniform within the X-ray beam’s field of view. Additionally, the X-ray tube voltage can also affect this nonuniformity. In this investigation, an intelligent technique based on the radial basis function neural network (RBFNN) is presented to predict the air kerma at every point within the fields of view of the X-ray beams of medical diagnostic imaging systems based on discrete and limited measured data. First, a diagnostic imaging system was modeled with the help of the Monte Carlo N Particle X version (MCNPX) code. It should be noted that a tungsten target and beryllium window with a thickness of 1 mm (no extra filter was applied) were used for modeling the X-ray tube. Second, the air kerma was calculated at various discrete positions within the conical X-ray beam for tube voltages of 40 kV, 60 kV, 80 kV, 100 kV, 120 kV, and 140 kV (this range covers most medical X-ray imaging applications) to provide the adequate dataset for training the network. The X-ray tube voltage and location of each point at which the air kerma was calculated were used as the RBFNN inputs. The calculated air kerma was also assigned as the output. The trained RBFNN model was capable of estimating the air kerma at any random position within the X-ray beam’s field of view for X-ray tube voltages within the range of medical diagnostic radiology (20–140 kV).

The ultimate manifestation of several heart diseases is heart failure, which is closely related to cardiac insufficiency, ventricular remodeling, and cytokine system activation. This study mainly assessed whether astragaloside regulates Caspase-3 by controlling Bcl-2/Bax pathway to protect cardiomyocytes in heart failure. Five groups were set up as model group, Bcl-2 inhibitor (ABT-199) group, Bax inhibitor (BIP-V5) group, low-dose and high-dose astragaloside group. Hematoxylin-eosin(HE) staining, CCK-8, Transwell method and flow cytometry measured histopathology of mouse myocardial tissue, proliferation, migration and apoptosis of cardiomyocytes respectively, and pathway-related genes, proteins and Caspase-3 levels were also measure. According to HE staining, the banding and cell swelling of three groups treated with astragaloside were significantly improved compared with model group, and the higher the concentration was, the more was significant improvement. Astragaloside inhibited Caspase-3 and Bax expressions and up-regulated Bcl-2 expression (all P < 0.05). The apoptosis of cardiomyocytes was related to Bcl-2 in the heart failure process, and apoptosis was controlled after using Bcl-2 mimics, but inhibition of Bax also showed a consistent trend. When Bcl-2/Bax ratio was increased, Caspase-3 was down-regulated. Astragaloside can promote increased Bcl-2/Bax ratio, mediate decreased Caspase-3 level in the cardiomyocytes, thereby inhibiting apoptosis. By increasing the concentration of astragaloside, the expression of Bcl-2/Bax can be up-regulated, which can further inhibit Caspase-3 expression, thereby reducing the damage of cardiomyocytes in heart failure tissue, and also inhibiting cell apoptosis.