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In a flat band superconductor, the charge carriers’ group velocity v F is extremely slow. Superconductivity therein is particularly intriguing, being related to the long-standing mysteries of high-temperature superconductors 1 and heavy-fermion systems 2 . Yet the emergence of superconductivity in flat bands would appear paradoxical, as a small v F in the conventional Bardeen–Cooper–Schrieffer theory implies vanishing coherence length, superfluid stiffness and critical current. Here, using twisted bilayer graphene 3 – 7 , we explore the profound effect of vanishingly small velocity in a superconducting Dirac flat band system 8 – 13 . Using Schwinger-limited non-linear transport studies 14 , 15 , we demonstrate an extremely slow normal state drift velocity v n  ≈ 1,000 m s –1 for filling fraction ν between −1/2 and −3/4 of the moiré superlattice. In the superconducting state, the same velocity limit constitutes a new limiting mechanism for the critical current, analogous to a relativistic superfluid 16 . Importantly, our measurement of superfluid stiffness, which controls the superconductor’s electrodynamic response, shows that it is not dominated by the kinetic energy but instead by the interaction-driven superconducting gap, consistent with recent theories on a quantum geometric contribution 8 – 12 . We find evidence for small Cooper pairs, characteristic of the Bardeen–Cooper–Schrieffer to Bose–Einstein condensation crossover 17 – 19 , with an unprecedented ratio of the superconducting transition temperature to the Fermi temperature exceeding unity and discuss how this arises for ultra-strong coupling superconductivity in ultra-flat Dirac bands. The authors investigate the effect of small velocity in a superconducting Dirac flat band system, finding evidence for small pairs and that superfluid stiffness is not dominated by kinetic energy.

For the unconventional superconducting phases in moire materials, a critical question is the role played by electronic interactions in the formation of Cooper pairs. In twisted bilayer graphene (tBLG), the strength of electronic interactions can be reduced by increasing the twist angle or screening provided by the dielectric medium. In this work, we place tBLG at 3-4 nm above bulk SrTiO3 substrates, which have a large yet tunable dielectric constant. By raising the dielectric constant in situ in a magic angle device, we observe suppression of both the height and the width of the entire superconducting dome, thus demonstrating that, unlike conventional superconductors, the pairing mechanism in tBLG is strongly dependent on electronic interactions. Interestingly, in contrast to the absence of superconductivity in devices on SiO2 with angle>1.3 deg, we observe a superconducting pocket in a large-angle (angle=1.4 deg) tBLG/STO device while the correlated insulating states are absent. These experimental results are in qualitative agreement with a theoretical model in which the pairing mechanism arises from Coulomb interactions that are screened by plasmons, electron-hole pairs, and longitudinal acoustic phonons. Our results highlight the unconventional nature of the superconductivity in tBLG, the double-edged role played by electronic interactions in its formation, as well as their complex interplay with the correlated insulating states.

The high-speed and high-precision motorized spindle is the future development trend of the CNC machine tool field, and has become the focus of research in the world. High-speed motorized spindles tend to develop in the direction of high precision, high speed, low energy consumption, high efficiency, and high reliability. We undertake a through, systematic review of the development history perspective of the research on precision bearing technology, dynamic balancing technology, thermal error measurement and compensation technology with regard to the key technologies of high-speed motorized spindles. On this basis, the current level of development of key technologies for high-speed motorized spindles is analyzed, and the objective advantages and disadvantages of existing technologies are summarized. Finally, the development tendency of high-speed motorized spindle technology is predicted and foreseen.

Based on accumulating evidence, patients recovering from mild and moderate traumatic brain injury (TBI) often experience increased sensitivity to stressful events. However, few studies have assessed on the effects and pathophysiological mechanisms of stress on TBI. In the current study, using a mouse model of moderate TBI, we investigated whether restraint stress (RS) regulates secondary neurodegeneration and neuronal cell death, which are commonly associated with neurological dysfunctions. Our data showed that RS significantly reduced body weight recovery, delayed the recovery of neurological functions (motor function, cognitive function and anxiety-like behavior) and exacerbated the brain lesion volume after moderate TBI. Immunofluorescence results indicated that moderate TBI-induced cell insults and blood–brain barrier leakage were aggravated by RS. Further Western blotting experiments showed that RS activated endoplasmic reticulum (ER) stress excessively after moderate TBI and decreased the number of NeuN-positive cells, but increased the number of CHOP/NeuN-co-positive cells by performing immunostaining in the injured cortex after moderate TBI. Moreover, RS increased the ratios of CHOP/Aβ and CHOP/p-Tau co-positive cells in the injured cortex after moderate TBI. However, blocking ER stress with the classic ER stress inhibitor salubrinal remarkably decreased apoptosis and the levels of autophagy-related proteins in the mouse model of moderate TBI plus RS. Collectively, RS delays the recovery of neurological function and deteriorates morphological damage by excessively activating ER stress-mediated neurodegeneration, apoptosis and autophagy after moderate TBI. Thus, monitoring stress levels in patients recovering from non-severe TBI may merit consideration in the future.

Household contacts (HHCs) of patients with active tuberculosis (ATB) are at higher risk of ( ) infection. However, the immune factors responsible for different defense responses in HHCs are unknown. Hence, we aimed to evaluate transcriptome signatures in human peripheral blood mononuclear cells (PBMCs) of HHCs to aid risk stratification. We recruited 112 HHCs of ATB patients and followed them for 6 years. Among the HHCs, only 2 developed ATB, while the remaining HHCs were classified into three groups: (1) HHC-1 group (  = 23): HHCs with consistently positive T-SPOT.TB test, negative chest radiograph, and no clinical symptoms or evidence of ATB during the 6-year follow-up period; (2) HHC-2 group (  = 15): HHCs with an initial positive T-SPOT result that later became negative without evidence of ATB; (3) HHC-3 group (  = 14): HHCs with a consistently negative T-SPOT.TB test and no clinical or radiological evidence of ATB. HHC-2 and HHC-3 were combined as HHC-23 group for analysis. RNA sequencing (RNA-seq) in PBMCs, with and without purified protein derivative (PPD) stimulation, identified significant differences in gene signatures between HHC-1 and HHC-23. Gene ontology analysis revealed functions related to bacterial pathogens, leukocyte chemotaxis, and inflammatory and cytokine responses. Modules associated with clinical features in the HHC-23 group were linked to the IL-17 signaling pathway, ferroptosis, complement and coagulation cascades, and the TNF signaling pathway. Validation using real-time PCR confirmed key genes like ATG-7, CXCL-3, and TNFRSF1B associated with infection outcomes in HHCs. Our research enhances understanding of disease mechanisms in HHCs. HHCs with persistent latent tuberculosis infection (HHC-1) showed significantly different gene expression compared to HHCs with no infection (HHC-23). These findings can help identify HHCs at risk of developing ATB and guide targeted public health interventions.

As one form of stroke, intracerebral hemorrhage (ICH) is a fatal cerebrovascular disease, which has high morbidity and mortality and lacks effective medical treatment. Increased infiltration of inflammatory cytokines coupled with pyroptotic cell death is involved in the pathophysiological process of ICH. However, little is known about whether concomitant fracture patients have the same progression of inflammation and pyroptosis. Hence, we respectively established the mouse ICH model and ICH with bilateral tibial fracture model (MI) to explore the potential cross-talk between the above two injuries. We found that MI obviously reversed the expressions of pyroptosis-associated proteins, which were remarkably up-regulated at the acute phase after ICH. Similar results were observed in neuronal expressions via double immunostaining. Furthermore, brain edema was also significantly alleviated in mice who suffered MI, when compared with ICH alone. To better clarify the potential mechanisms that mediated this cross-talk, recombinant mouse interleukin-13 (IL-13) was used to investigate its effect on pyroptosis in the mouse MI model, in which a lower level of IL-13 was observed. Remarkably, IL-13 administration re-awakened cell death, which was mirrored by the re-upregulation of pyroptosis-associated proteins and PI-positive cell counts. The results of hemorrhage volume and behavioral tests further confirmed its critical role in regulating neurological functions. Besides, the IL-13-treated MI group showed poor outcomes of fracture healing. To sum up, our research indicates that controlling the IL-13 content in the acute phase would be a promising target in influencing the outcomes of brain injury and fracture, and meanwhile, provides new evidence in repairing compound injuries in clinics.

Bafilomycin C1, which was isolated from Streptomyces albolongus in our previous work, exhibited strong cytotoxicity against several cancer cell lines. This study aimed to evaluate its antitumor effect on human hepatocellular cancer SMMC7721 cells and the underlying mechanism in vitro and in vivo. MTT assay revealed that bafilomycin C1 retarded SMMC7721 cell growth and proliferation. Western blot and real-time qPCR analysis revealed that bafilomycin C1 caused partial G0/G1 phase cell-cycle arrest, downregulated the expression of cyclin D3, cyclin E1, CDK2, CDK4, and CDK6 and upregulated the expression of p21. Moreover, bafilomycin C1 caused mitochondrial membrane dysfunction through oxidative stress. Furthermore, bafilomycin C1 decreased the expression of Bcl-2; increased the expression of Bax, p53, and P-p53; and increased cleavage of caspase-9 and caspase-3, thereby inducing the intrinsic caspase-dependent apoptotic pathway. In vivo experiments in mice suggested that bafilomycin C1 suppressed tumor growth with few side effects. Cell-cycle arrest and induced apoptosis in tumor tissues in a mouse model treated with bafilomycin C1 were demonstrated by histological analyses, western blot and TUNEL. These findings indicate that bafilomycin C1 may be a promising candidate for hepatic cellular cancer therapy.

To find the genetic markers related to the antipsychotic-induced weight gain (AIWG), we analyzed associations among candidate gene single-nucleotide polymorphisms (SNPs) and quantitative traits of weight changes and lipid profiles in a Chinese Han population. A total of 339 schizophrenic patients, including 86 first-episode patients (FEPs), meeting the entry criteria were collected. All patients received atypical antipsychotic drug monotherapy and hospitalization and were followed for 12 weeks. Forty-three SNPs in 23 candidate genes were calculated for quantitative genetic association with AIWG, performed by PLINK. The TOX gene SNP rs11777927 ( P  = 0.009) and the ADIPOQ gene SNP rs182052 ( P  = 0.019) were associated with AIWG (in body mass index, BMI). In addition, the BDNF SNP rs6265 ( P  = 0.002), BDAF SNP rs11030104 SNP ( P  = 0.001), and ADIPOQ SNPs rs822396 ( P  = 0.003) were significantly associated with the change of waist-to-hip ratio (WHR) induced by atypical antipsychotics. These results were still significant after age and gender adjustments. These findings provide preliminary evidence supporting the role of TOX, ADIPOQ and BDNF in weight and WHR gain induced by atypical antipsychotics.