A visible-light-promoted transfer hydrogenation of azobenzenes has been developed. In the presence of B2pin2 and upon visible-light irradiation, the reactions proceeded smoothly in methanol at ...ambient temperature. The azobenzenes with diverse functional groups have been reduced to the corresponding hydrazobenzenes with a yield of up to 96%. Preliminary mechanistic studies indicated that the hydrogen atom comes from the solvent and the transformation is achieved through a radical pathway.
Autophagy is related to the development of several tumors including acute myeloid leukemia (AML). Inhibition of autophagy in AML cells can make them more susceptible to chemotherapy. However, the ...influence of autophagy in mesenchymal stem cells (MSCs) remains inconclusive. In the present study, we demonstrated that the expression of ATG5 and autophagy were elevated in MSCs derived from AML patients (AML-MSCs) compared to healthy donors (HD-MSCs). After inhibiting autophagy by 3-Methyladenine (3 MA) or silencing ATG5, the differentiation potential of AML-MSCs was decreased, the fraction of G0/G1 phase was increased while that of G2 phase was reduced, and the expression of CXCL12 was reduced in AML-MSCs. After co-culture of NB4 and THP1 with MSCs pretreated with 3 MA or ATG5 knockdown respectively, the sensitivity of AML cell lines to daunorubicin and doxorubicin was improved in a dose- and time-dependent manner compared to controls. The increased sensitivity of AML cells to genotoxic agents was related to ERK1/2 and AKT pathway. These results suggested ATG5 mediated potential differentiation capacities and cell cycle distribution of AML-MSCs, and targeting autophagy, especially ATG5 in AML-MSCs could improve the chemosensitivity of AML.
•The expression of ATG5 and autophagy were elevated in AML-MSCs.•Inhibition of autophagy reduced the potential differentiation capacities of AML-MSCs.•Cell cycle distribution was altered after inhibition of autophagy in AML-MSCs.•Autophagy in MSCs affected the sensitivity of AML cell lines to genotoxic agents.•Autophagy in MSCs affected chemosensitivity of AML cells via ERK1/2 and AKT pathway.
For tomographic reconstruction in combustion diagnostics, it is usually necessary to solve a rank-deficient problem, where the number of non-linear dependent equations is smaller than the number of ...unknowns. In some reconstructions, there are grids without rays passing through. This produces artifacts during the reconstruction. In this paper, the weight of the regulation equation is modified with the number of the rays crossing the grid cells. The effect of the neighboring grid values as well as the number of rays crossing the grid cells is considered in the new regulation method. Numerical simulation results show that the new regulation method suppresses the reconstruction error of the no rays crossing grid and successfully restrains the corner distortion in four projection angles. The effects of the weight coefficient and the smoothing factor on the reconstruction are examined through a numerical study. Finally, a combustion experiment demonstrates that the new regulation method can significantly reduce the reconstructed error, especially for the non-ray crossing condition, and the results are compared with thermocouple measurements and reconstructions without modified regulation.
Summary
The leukaemic bone marrow microenvironment, comprising abnormal mesenchymal stromal cells (MSCs), is responsible for the poor prognosis of acute myeloid leukaemia (AML). Therefore, it is ...essential to determine the mechanisms underlying the supportive role of MSCs in the survival of leukaemia cells. Through in silico analyses, we identified a total of 271 aberrantly expressed genes in the MSCs derived from acute myeloid leukemia (AML) patients that were associated with adipogenic differentiation, of which aldo‐keto reductase 1C1 (AKR1C1) was significantly upregulated in the AML‐MSCs. Knockdown of AKR1C1 in the MSCs suppressed adipogenesis and promoted osteogenesis, and inhibited the growth of co‐cultured AML cell lines compared to the situation in wild‐ type AML‐derived MSCs. Introduction of recombinant human AKR1C1 in the MSCs partially alleviated the effects of AKR1C1 knockdown. In addition, the absence of AKR1C1 reduced secretion of cytokines such as MCP‐1, IL‐6 and G‐CSF from the MSCs, along with inactivation of STAT3 and ERK1/2 in the co‐cultured AML cells. AKR1C1 is an essential factor driving the adipogenic differentiation of leukaemic MSCs and mediates its pro‐survival effects on AML cells by promoting cytokine secretion and activating the downstream pathways in the AML cells.
Objective. Pediatric asthma is still a health threat to the children. Long noncoding RNA-NEAT1 (lncRNA-NEAT1) was reported to be positively correlated with the severity of asthma. We aimed to study ...the effects and mechanism of lncRNA-NEAT1on inflammatory reaction and phenotypic transformation of airway smooth muscle cells (ASMCs) in the bronchial asthma. Method. The degree of lncRNA-NEAT1 and miR-128 mRNA in children with bronchial asthma and healthy individuals was tested by qRT-PCR. After the inflammatory reaction and phenotypic transformation of PDGF-BB-induced ASMCs, the expression of lncRNA-NEAT1 or miR-128 in the AMSC was disturbed in the AMSC. Subsequently, the expression of lncRNA-NEAT1 and miR-128 was detected by the way of qRT-PCR, and western blot was applied to measure the expression of MMP-2, MMP-9, α-SMA, calponin, NF-κB, and so on in the cells. The content of TNF-α, IL-1β, IL-6, and IL-8 in the cell culture supernatant was checked by ELISA. MTT, Transwell, and flow cytometry were used to detect cell proliferation, migration, and apoptosis. Further, the targeting relations between lncRNA-NEAT1 and miR-128 were evaluated by the dual-luciferase reporter assay. Result. In the sputum of children with bronchial asthma, lncRNA-NEAT1 was significantly upregulated while miR-128 was rapidly downregulated. Besides, lncRNA-NEAT1 and miR-128 were competitively combined and, for their expression, negatively correlated. Conclusion. lncRNA-NEAT1 sponges miR-128 to boost PDGF-BB-induced inflammatory reaction and phenotypic transformation of ASMCs to aggravate the occurrence and development of childhood bronchial asthma.
BACKGROUNDTo screen risk factors for the recurrence in children with Henoch-Schönlein Purpura (HSP) and to develop and validate a nomogram for recurrence in children with HSP. METHODSDuring September ...2019 and September 2021, 212 children with HSP were selected in this study. The children were divided into two sets in a proportion of 7:3 using R language, with the first group as the training sets and the second as the internal validation sets. The related variables were analyzed by univariate and multivariate logistic regression analyses, and a nomogram for predicting the recurrence in HSP children was established. The nomogram was evaluated by ROC curve, calibration curve and decision curve, and 1000 times bootstrap resampling method was used to verify the model internally. RESULTSUnivariate and multivariate regression analyses identified respiratory infection, without preventive medication and diet restriction, age, allergen positive and abnormal urine routine as risk factors for the recurrence in children with HSP. Those risk factors were used to construct a predictive nomogram. The calibration curves revealed excellent accuracy of the predictive nomogram model, internally and externally. CONCLUSIONSWe constructed and validated a clinical nomogram to predict the recurrence in children with HSP. We confirmed that respiratory tract infection, without preventive medication and diet restriction, age, allergen positive and abnormal urine routine were independent recurrence risk factors. This nomogram had a good performance in clinical decision-making.
Acute myeloid leukemia (AML) blasts release a wide range of chemokines in which CXCL8 has recently been recognized to be important for tumor progression. To find out the function of CXCL8 in AML, we ...compared blood serum of AML patients and healthy donors and found that the average level of CXCL8 was higher in AML patients. Among patients, higher expression of CXCL8 was also a positive recurrence indicator which illustrated the critical role of CXCL8 in AML. Knocking down of CXCL8 in leukemic cell lines led to significant reduction of proliferation via inducing G0/G1 cell cycle arrest and apoptosis, which was accompanied by the inactivation of ERK1/2. Furthermore, inhibition of ERK1/2 by specific chemical inhibitors reconstructed the CXCL8 knocking down phenomenon. Overall, we demonstrated that expression level of CXCL8 had a positive relationship with recurrence probability in AML. And CXCL8 was strongly implicated in AML cells growth by activating the ERK1/2 signal pathway.
•CXCL8 is significantly up-regulated in AML and correlates with poor prognosis.•CXCL8 promotes proliferation in AML cell lines by affecting cell cycle and apoptosis.•CXCL8 influences proliferation through ERK1/2 pathway.
We extend the Becker-Tomes model to a rural economy with farm-nonfarm occupational dualism to study intergenerational educational mobility in rural China and India. Using data free of coresidency ...bias, we find that fathers’ nonfarm occupation and education were complementary in determining sons schooling in India, but separable in China. Sons faced lower mobility in India irrespective of fathers’ occupation. Sensitivity analysis using the Altonji et al. (J. Polit. Econ.
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(1), 151–84, 2005) approach suggests that genetic correlations alone could explain the intergenerational persistence in China, but not in India. Farm-nonfarm differences in returns to education, and geographic mobility are plausible mechanisms behind the contrasting cross-country evidence.
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