Mesenchymal stem cells (MSCs) protect the endothelial barrier complex and survival, implicated in the pathogenesis of acute lung injury (ALI) via paracrine hepatocyte growth factor (HGF). However, the mechanism of HGF in endothelial regulation remains unclear. Here, we introduced a coculture protocol of pulmonary microvascular endothelial cells (PMVECs)

Curcumin, the active component of turmeric, has been shown to protect against carcinogenesis and prevent tumor development in cancer. In our study, we tested the efficacy of a synthetic curcumin analogue, known as hydrazinocurcumin (HC), in breast cancer cells. The results demonstrated that compared to curcumin, HC was more effective in inhibiting STAT3 phosphorylation and downregulation of an array of STAT3 downstream targets which contributed to suppression of cell proliferation, loss of colony formation, depression of cell migration and invasion as well as induction of cell apoptosis. It was concluded that HC is a potent agent in the inhibition of STAT3 with more favorable pharmacological activity than curcumin, and HC may have translational potential as an effective cancer therapeutic or preventive agent for human breast carcinoma.

Background: T helper 17 cells (Th17)/regulatory T cells (Treg), as subtypes of CD4 + T cells, play an important role in the inflammatory response of acute respiratory distress syndrome (ARDS). However, there is still a lack of effective methods to regulate the differentiation balance of Th17/Treg. It was proven that mesenchymal stem cells (MSCs) could regulate the differentiation of CD4 + T cells, but the mechanism is still unclear. TGFβ1, a paracrine cytokine of MSCs, could also regulate the differentiation of Th17/Treg but is lowly expressed in MSCs. Therefore, mouse MSCs (mMSCs) overexpressing TGFβ1 were constructed by lentivirus transduction and intratracheally transplanted into LPS-induced ARDS mice in our study. The aim of this study was to evaluate the therapeutic effects of mMSCs overexpressing TGFβ1 on inflammation and immunoregulation by impacting the Th17/Treg balance in LPS-induced ARDS mice. Methods: mMSCs overexpressing TGFβ1 were constructed using lentiviral vectors. Then, mouse bone-marrowderived MSCs (mBM-MSC) and mBM-MSC-TGFβ1 (mBM-MSC overexpressing TGFβ1) were transplanted intratracheally into ARDS mice induced by lipopolysaccharide. At 3 and 7 days after transplantation, the mice were sacrificed, and the homing of the mMSCs was assayed by ex vivo optical imaging. The relative numbers of Th17 and Treg in the lungs and spleens of mice were detected by FCM. IL-17A and IL-10 levels in the lungs of mice were analysed by western blot. Permeability and inflammatory cytokines were evaluated by analysing the protein concentration of BALF using ELISA. Histopathology of the lungs was assessed by haematoxylin and eosin staining and lung injury scoring. Alveolar lung fibrosis was assessed by Masson's trichrome staining and Ashcroft scoring. The mortality of ARDS mice was followed until 7 days after transplantation. Results: The transduction efficiencies mediated by the lentiviral vectors ranged from 82.3 to 88.6%. Overexpressing TGFβ1 inhibited the proliferation of mMSCs during days 5-7 (p < 0.05) but had no effect on mMSC differentiation or migration (p > 0.05). Compared to that in the LPS + mBM-MSC-NC group mice, engraftment of mMSCs overexpressing TGFβ1 led to much more differentiation of T cells into Th17 or Treg (p < 0.05), improved permeability of injured lungs (p < 0.05) and ameliorative histopathology of lung tissue in

Renal fibrosis is defined as the excessive deposition and modification of extracellular matrix (ECM) in the renal parenchyma in response to injury and inflammation, resulting in renal function loss. This condition is common to many chronic kidney diseases occurring under diverse pathological conditions, such as diabetic and hypertensive nephropathy. Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid metabolite involved in the regulation of cardiovascular functions and the pathogenesis of various cardiovascular diseases. S1P has also been considered an important regulator of fibrotic diseases, playing significant roles in the differentiation of fibroblasts to myofibroblasts and in the induction of inflammatory responses during the early stages of fibrotic diseases. This minireview summarizes recent research findings regarding the importance of the sphingosine kinase-1-S1P-S1P receptor axis and its interactions with other classic fibrotic signaling pathways and the immune inflammatory response to reveal novel therapeutic targets for the treatment or prevention of renal fibrosis.

1 We study the problem of interference source identification, through the lens of recognizing one of 15 different channels that belong to 3 different wireless technologies: Bluetooth, Zigbee, and WiFi. We employ deep learning algorithms trained on received samples taken from a 10 MHz band in the 2.4 GHz ISM Band. We obtain a classification accuracy of around 89.5% using any of four different deep neural network architectures: CNN, ResNet, CLDNN, and LSTM, which demonstrate the generality of the effectiveness of deep learning at the considered task. Interestingly, our proposed CNN architecture requires approximately 60% of the training time required by the state of the art while achieving slightly larger classification accuracy. We then focus on the CNN architecture and further optimize its training time while incurring minimal loss in classification accuracy using three different approaches: 1-Band Selection, where we only use samples belonging to the lower and uppermost 2 MHz bands, 2-SNR Selection, where we only use training samples belonging to a single SNR value, and 3-Sample Selection, where we try various sub-Nyquist sampling methods to select the subset of samples most relevant to the classification task. Our results confirm the feasibility of fast deep learning for wireless interference identification, by showing that the training time can be reduced by as much as 30x with minimal loss in accuracy.