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In 'Fou Lei: An Insistence on Truth', Mingyuan Hu thinks through the life and work of one of modern China's most significant public intellectuals, investigating his Shanghai-Paris trajectory and his resistance against cultural barbarism. Using hitherto undiscovered archival documents, Hu presents the first study of Fou Lei's youth, particularly his formative years in Europe (1928-1931), and analyses the critic-translator's identity vis-لa-vis intercultural friendships and political predicaments. Bringing together previously untranslated material in French and Chinese, 'Fou Lei' paints a man in dark times searching for illumination through words, and invites the reader to reconsider questions, unresolved and unspoken, about his tragic end.

Mesenchymal stem cells (MSCs) are a population of multipotent cells with a superior ability to promote tissue repair by regulating regeneration and inflammation. Effective application of MSCs in disease treatment relies on the production of relatively homogeneous cell population. However, the cellular heterogeneity and the differentiation trajectories of in vitro expanded MSCs remain largely unclear. We profiled the transcriptomes of 361 single MSCs derived from two umbilical cords (UC-MSCs). These UC-MSCs were harvested at different passages and stimulated with or without inflammatory cytokines. Weighted gene correlation network analysis revealed that UC-MSCs surprisingly possess only limited heterogeneity, regardless of donors, and passages. We also found that upon pretreatment with inflammatory cytokines (IFNγ and TNFα), a classical strategy that can improve the efficiency of MSC-based therapy, MSCs exhibited uniformed changes in gene expression. Cell cycle-based principal component analysis showed that the limited heterogeneity identified in these UC-MSCs was strongly associated with their entrance into the G2/M phase. This was further proven by the observation that one featured gene, CD168, was expressed in a cell cycle-dependent manner. When CD168 high UC-MSCs were sorted and cultured in vitro, they again showed similar CD168 expression patterns. Our results demonstrated that in vitro expanded UC-MSCs are a well-organized population with limited heterogeneity dominated by cell cycle status. Thus, our studies provided information for standardization of MSCs for disease treatment.

The guest room and aisle of electric high-speed maglev train must be shielded from leakage magnetic flux produced by superconducting strong magnetic field. To reduce magnetic leakage, the superconducting magnetic levitation system structure is obtained by extended lagrangian optimization method. The optimized superconducting coil structure has the advantages of reducing magnetic leakage, improving magnetic field utilization, reducing the weight of the magnetic isolation plate and the weight of the maglev train, and enhancing the load-bearing capacity of the maglev train. Based on optimized superconducting coil parameters for high-speed maglev, the magnetic shielding effect at the aisle and the guest room, the magnetic flux density distribution at the magnetic shielding is calculated and analyzed through analytical calculation. The relevant conclusions indicate that the magnetic suspension structure has the advantages of reducing end coil leakage flux and the weight of the high-speed maglev train.

Cancer treatments have been revolutionized by the emergence of immune checkpoint blockade therapies. However, only a minority of patients with various tumor types have benefited from such treatments. New strategies focusing on the immune contexture of the tumor tissue microenvironment hold great promises. Here, we created IFNα-overexpressing mesenchymal stromal cells (IFNα-MSCs). Upon direct injection into tumors, we found that these cells are powerful in eliminating several types of tumors. Interestingly, the intra-tumoral injection of IFNα-MSCs could also induce specific anti-tumor effects on distant tumors. These IFNα-MSCs promoted tumor cells to produce CXCL10, which in turn potentiates the infiltration of CD8 + T cells in the tumor site. Furthermore, IFNα-MSCs enhanced the expression of granzyme B (GZMB) in CD8 + T cells and invigorated their cytotoxicity in a Stat3-dependent manner. Genetic ablation of Stat3 in CD8 + T cells impaired the effect of IFNα-MSCs on GZMB expression. Importantly, the combination of IFNα-MSCs and PD-L1 blockade induced an even stronger anti-tumor immunity. Therefore, IFNα-MSCs represent a novel tumor immunotherapy strategy, especially when combined with PD-L1 blockade.

Inorganic plastic semiconductors play a crucial role in the realm of flexible electronics. In this study, we present a cost-effective plastic thermoelectric semimetal magnesium bismuthide ( α -Mg 3 Bi 2 ), exhibiting remarkable thermoelectric performance. Bulk single-crystalline α -Mg 3 Bi 2 exhibits considerable plastic deformation at room temperature, allowing for the fabrication of intricate shapes such as the letters “SUSTECH” and a flexible chain. Transmission electron microscopy, time-of-flight neutron diffraction, and chemical bonding theoretic analyses elucidate that the plasticity of α -Mg 3 Bi 2 stems from the helical dislocation-driven interlayer slip, small-sized Mg atoms induced weak interlayer Mg-Bi bonds, and low modulus of intralayer Mg 2 Bi 2 2- networks. Moreover, we achieve a power factor value of up to 26.2 µW cm -1 K -2 along the c-axis at room temperature in an n-type α -Mg 3 Bi 2 crystal. Our out-of-plane flexible thermoelectric generator exhibit a normalized power density of 8.1 μW cm -2 K -2 with a temperature difference of 7.3 K. This high-performance plastic thermoelectric semimetal promises to advance the field of flexible and deformable electronics. The authors find that the plasticity of magnesium bismuthide (α-Mg 3 Bi 2 ) arises from helical dislocation-driven interlayer slip, and the dispersion of lightweight Mg atoms also plays a pivotal role in facilitating strain redistribution during plastic deformation.

Background To evaluate the association and dose–response relationship between polyunsaturated fatty acid (PUFA) intake and incidence of type 2 diabetes (T2D) in adults. Methods PubMed, Embase, Cochrane Library, and Web of Science databases were searched for cohort studies that examined the association between PUFA and T2D incidence published up to September 6, 2021. Relative risk (RR) or hazard ratio (HR) was used as the effect indicator, each effect size was expressed by 95% confidence interval (CI). The presence of heterogeneity of effect size between studies was assessed by the Q-test and I 2 statistics. If I 2  ≥ 50%, the random-effects model was applied, otherwise the fixed effects model was used. Sensitivity analysis was performed for all models. Potential publication bias was assessed. We conducted linear and nonlinear dose–response meta-analyses, calculated summary relative risk (SRR). Results Twenty-five articles were selected including 54,000 patients in this study. Our estimates observed no linear associations between total PUFA and the incidence of T2D. However, the summary dose–response curve of T2D risk increased in a nonlinear pattern with the consumption of omega-3 PUFA ( P nonlinearity  < 0.001) and docosahexaenoic acid (DHA) ( P nonlinearity  = 0.040). Our subgroup analysis showed that total PUFA intake was associated with increased incidence of T2D in Europe (RR: 1.040, 95% CI 1.009 to 1.072), and Australia (RR: 1.188, 95% CI 1.113 to 1.269). However, total PUFA intake was associated with decreased T2D incidence in Asia (RR: 0.897, 95% CI 0.860 to 0.936). Subgroup analysis based on PUFA types showed that DHA intake was associated with decreased T2D incidence (RR: 1.164, 95% CI 1.048 to 1.294) while linoleic acid (LA) decreased T2D incidence (RR: 0.956, 95% CI 0.930 to 0.983). Regarding the sex subgroup, women’s intake of total PUFA would increase the risk of T2D (RR: 1.049, 95% CI 1.019 to 1.079) while total PUFA intake decreased the risk of T2D in men (RR: 0.955, 95% CI 0.913 to 0.999). Conclusion For specific PUFA, dose–response curves show nonlinear significant associations between PUFA intakes and T2D. It may be necessary to pay attention to the effects of PUFA and type of intake on T2D. Trial registration Not applicable

Preadipocytes can give rise to either white adipocytes or beige adipocytes. Owing to their distinct abilities in nutrient storage and energy expenditure, strategies that specifically promote “beiging” of adipocytes hold great promise for counterbalancing obesity and metabolic diseases. Yet, factors dictating the differentiation fate of adipocyte progenitors remain to be elucidated. We found that stearoyl-coenzyme A desaturase 1 (Scd1)-deficient mice, which resist metabolic stress, possess augmentation in beige adipocytes under basal conditions. Deletion of Scd1 in mature adipocytes expressing Fabp4 or Ucp1 did not affect thermogenesis in mice. Rather, Scd1 deficiency shifted the differentiation fate of preadipocytes from white adipogenesis to beige adipogenesis. Such effects are dependent on succinate accumulation in adipocyte progenitors, which fuels mitochondrial complex II activity. Suppression of mitochondrial complex II by Atpenin A5 or oxaloacetic acid reverted the differentiation potential of Scd1-deficient preadipocytes to white adipocytes. Furthermore, supplementation of succinate was found to increase beige adipocyte differentiation both in vitro and in vivo. Our data reveal an unappreciated role of Scd1 in determining the cell fate of adipocyte progenitors through succinate-dependent regulation of mitochondrial complex II.

Aiming at the control performance degradation of permanent magnet synchronous motor (PMSM) drive systems caused by uncertainties of internal and external disturbances, a robust control algorithm integrating an improved fast terminal sliding mode (IFTSM) surface with a novel adaptive reaching law (NARL) is proposed. A dynamic model of PMSM with disturbances is established, and an improved fast terminal sliding mode surface is designed. By introducing nonlinear terms and error derivative feedback mechanisms, the finite-time rapid convergence of system states is achieved, while solving the singularity problem of traditional terminal sliding mode control. Combined with the novel adaptive reaching law strategy, a state-dependent gain adjustment function is used to dynamically optimize the balance between reaching speed and chattering, enhancing the smoothness of the system′s dynamic response. Through the synergy of the finite-time convergence characteristic of the improved sliding mode surface and the novel adaptive reaching law, the proposed algorithm significantly enhances the system′s anti-interference capability against load mutations and parameter time variations. Experiment results demonstrate that under complex working conditions, the algorithm achieves superior speed tracking accuracy and current stability, providing a control solution with strong anti-interference capability and fast response for PMSM speed control systems.

p53 plays a pivotal role in controlling the differentiation of mesenchymal stem cells (MSCs) by regulating genes involved in cell cycle and early steps of differentiation process. In the context of osteogenic differentiation of MSCs and bone homeostasis, the osteoprotegerin/receptor activator of NF-κB ligand/receptor activator of NF-κB (OPG/RANKL/RANK) axis is a critical signaling pathway. The absence or loss of function of p53 has been implicated in aberrant osteogenic differentiation of MSCs that results in higher bone formation versus erosion, leading to an unbalanced bone remodeling. Here, we show by microCT that mice with p53 deletion systemically or specifically in mesenchymal cells possess significantly higher bone density than their respective littermate controls. There is a negative correlation between p53 and OPG both in vivo by analysis of serum from p53 +/+ , p53 +/− , and p53 −/− mice and in vitro by p53 knockdown and ChIP assay in MSCs. Notably, high expression of Opg or its combination with low level of p53 are prominent features in clinical cancer lesion of osteosarcoma and prostate cancer respectively, which correlate with poor survival. Intra-bone marrow injection of prostate cancer cells, together with androgen can suppress p53 expression and enhance local Opg expression, leading to an enhancement of bone density. Our results support the notion that MSCs, as osteoblast progenitor cells and one major component of bone microenvironment, represent a cellular source of OPG, whose amount is regulated by the p53 status. It also highlights a key role for the p53-OPG axis in regulating the cancer associated bone remodeling.