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The Griffiths singularity in a phase transition, caused by disorder effects, was predicted more than 40 years ago. Its signature, the divergence of the dynamical critical exponent, is challenging to observe experimentally. We report the experimental observation of the quantum Griffiths singularity in a two-dimensional superconducting system. We measured the transport properties of atomically thin gallium films and found that the films undergo superconductor-metal transitions with increasing magnetic field. Approaching the zero-temperature quantum critical point, we observed divergence of the dynamical critical exponent, which is consistent with the Griffiths singularity behavior. We interpret the observed superconductor-metal quantum phase transition as the infinite-randomness critical point, where the properties of the system are controlled by rare large superconducting regions.

Background Ventilator-induced lung injury (VILI) is caused by overdistension of the alveoli by the repetitive recruitment and derecruitment of alveolar units. This study aims to investigate the potential role and mechanism of fibroblast growth factor 21 (FGF21), a metabolic regulator secreted by the liver, in VILI development. Methods Serum FGF21 concentrations were determined in patients undergoing mechanical ventilation during general anesthesia and in a mouse VILI model. Lung injury was compared between FGF21-knockout (KO) mice and wild-type (WT) mice. Recombinant FGF21 was administrated in vivo and in vitro to determine its therapeutic effect. Results Serum FGF21 levels in patients and mice with VILI were significantly higher than in those without VILI. Additionally, the increment of serum FGF21 in anesthesia patients was positively correlated with the duration of ventilation. VILI was aggravated in FGF21-KO mice compared with WT mice. Conversely, the administration of FGF21 alleviated VILI in both mouse and cell models. FGF21 reduced Caspase-1 activity, suppressed the mRNA levels of Nlrp3 , Asc, Il-1β, Il-18, Hmgb1 and Nf-κb , and decreased the protein levels of NLRP3, ASC, IL-1β, IL-18, HMGB1 and the cleaved form of GSDMD. Conclusions Our findings reveal that endogenous FGF21 signaling is triggered in response to VILI, which protects against VILI by inhibiting the NLRP3/Caspase-1/GSDMD pyroptosis pathway. These results suggest that boosting endogenous FGF21 or the administration of recombinant FGF21 could be promising therapeutic strategies for the treatment of VILI during anesthesia or critical care.

Prostaglandin E receptor subtype 4 (EP4) is widely distributed in the heart, but its role in hepatic ischemia/reperfusion (I/R), particularly in mitochondrial permeability transition pore (MPTP) modulation, is yet to be elucidated. In the present study, an EP4 agonist (CAY10598) was used in a rat model to evaluate the effects of EP4 activation on liver I/R and the mechanisms underlying this. I/R insult upregulated hepatic EP4 expression during early reperfusion. In addition, subcutaneous CAY10598 injection prior to the onset of reperfusion significantly increased hepatocyte cAMP concentrations and decreased serum ALT and AST levels and necrotic and apoptotic cell percentages, after 6 h of reperfusion. Moreover, CAY10598 protected mitochondrial morphology, markedly inhibited mitochondrial permeability transition pore (MPTP) opening and decreased liver reactive oxygen species levels. This occurred via activation of the ERK1/2-GSK3β pathway rather than the janus kinase (JAK)2-signal transducers and activators of transcription (STAT)3 pathway, and resulted in prevention of mitochondria-associated cell injury. The MPTP opener carboxyatractyloside (CATR) and the ERK1/2 inhibitor PD98059 also partially reversed the protective effects of CAY10598 on the liver and mitochondria. The current findings indicate that EP4 activation induces ERK1/2-GSK3β signaling and subsequent MPTP inhibition to provide hepatoprotection, and these observations are informative for developing new molecular targets and preventative therapies for I/R in a clinical setting.

A bstract The Efimov effect is an intriguing three-body quantum phenomenon. Searching for Efimov states within the realms of nuclear and hadronic physics presents a challenge due to the inherent inability of natural physical systems to exhibit adjustable two-body scattering lengths. In this study, we examine the potential existence of Efimov states in the D * D * D * and DD * D * three-hadron systems. Utilizing a pionless effective field theory framework, we determine that the presence of Efimov states in the spectrum of the D * D * D * system is contingent upon the existence of an ( I, J ) = (1 , 2) D * D * two-body bound system. If only the T cc + and its heavy quark spin partner T cc ∗ + exist while there is no near-threshold pole in all other S -wave D (*) D * scattering amplitudes, no Efimov effect is expected in the D (*) D * D * systems.

Propofol pretreatment before reperfusion, or propofol conditioning, has been shown to be cardioprotective, while its mechanism is unclear. The current study investigated the roles of endocannabinoid signaling in propofol cardioprotection in an in vivo model of myocardial ischemia/reperfusion (I/R) injury and in in vitro primary cardiomyocyte hypoxia/reoxygenation (H/R) injury. The results showed that propofol conditioning increased both serum and cell culture media concentrations of endocannabinoids including anandamide (AEA) and 2-arachidonoylglycerol (2-AG) detected by LC-MS/MS. The reductions of myocardial infarct size in vivo and cardiomyocyte apoptosis and death in vitro were accompanied with attenuations of oxidative injuries manifested as decreased reactive oxygen species (ROS), malonaldehyde (MDA), and MPO (myeloperoxidase) and increased superoxide dismutase (SOD) production. These effects were mimicked by either URB597, a selective endocannabinoids degradation inhibitor, or VDM11, a selective endocannabinoids reuptake inhibitor. In vivo study further validated that the cardioprotective and antioxidative effects of propofol were reversed by selective CB2 receptor antagonist AM630 but not CB1 receptor antagonist AM251. We concluded that enhancing endogenous endocannabinoid release and subsequent activation of CB2 receptor signaling represent a major mechanism whereby propofol conditioning confers antioxidative and cardioprotective effects against myocardial I/R injury.

This Magnesium (Mg) alloys have been increasingly used in the automotive industry due to their superior mechanical properties compared with other metals. While there are some obstacles in the application of Mg alloy, one of that is its complex dynamic response characteristic. Many papers have studied the tensile and compression properties of AZ31B Mg alloys sheet, but lack of shear test. This paper presents experimental study, including the test method and test data analysis, on the AZ31B Mg alloy sheet. Uniaxial tension tests were carried out over a wide range of strain rates from to , which are of interest in vehicle crash CAE. At the same time uniaxial compression and shear tests at strain rates from to were also carried out. The different mechanical behavior of AZ31B Mg alloys sheet between tensile, compression and shear stress states can also be studied in this paper.

NYGGF4 , also known as phosphotyrosine interaction domain containing 1( PID1 ), is a recently discovered gene which is involved in obesity-related insulin resistance (IR) and mitochondrial dysfunction. We aimed to further elucidate the effects and mechanisms underlying NYGGF4-induced IR by investigating the effect of overexpressing mitochondrial transcription factor A (TFAM), which is essential for mitochondrial DNA transcription and replication, on NYGGF4-induced IR and mitochondrial abnormalities in 3T3-L1 adipocytes. Overexpression of TFAM increased the mitochondrial copy number and ATP content in both control 3T3-L1 adipocytes and NYGGF4-overexpressing adipocytes. Reactive oxygen species (ROS) production was enhanced in NYGGF4-overexpressing adipocytes and reduced in TFAM-overexpressing adipocytes; co-overexpression of TFAM significantly attenuated ROS production in NYGGF4-overexpressing adipocytes. However, overexpression of TFAM did not affect the mitochondrial transmembrane potential (ΔΨm) in control 3T3-L1 adipocytes or NYGGF4-overexpressing adipocytes. In addition, co-overexpression of TFAM-enhanced insulin-stimulated glucose uptake by increasing Glucose transporter type 4 (GLUT4) translocation to the PM in NYGGF4-overexpressing adipocytes. Overexpression of NYGGF4 significantly inhibited tyrosine phosphorylation of Insulin receptor substrate 1 (IRS-1) and serine phosphorylation of Akt, whereas overexpression of TFAM strongly induced phosphorylation of IRS-1 and Akt in NYGGF4-overexpressing adipocytes. This study demonstrates that NYGGF4 plays a role in IR by impairing mitochondrial function, and that overexpression of TFAM can restore mitochondrial function to normal levels in NYGGF4-overexpressing adipocytes via activation of the IRS-1/PI3K/Akt signaling pathway.

Through simulating interaction between pile and foundation soil after establishing surface-surface contact element with finite element method and ANSYS software, the load resistance performance and ultimate strength of the ground anchor pile working for a workover derrick are achieved. In winter, frozen soil depth can be up to 2 meters in north china. When temperature rises in spring, the Polar grassland changes by three stages, namely, frozen, freeze thawing and melted. But for the large temperature difference between morning and evening, the state of the soil layer is extremely unstable which greatly affect the carrying capacity of anchor piles. This paper focuses on the melting influence of soil layer and the load resistance performance is studied. With a set of calculation parameter, the simulation result shows that the carrying capacity of anchor piles decreases 28% in melted state than freeze thawing.

the workover rig is always fixed by anchor piles in land oilfields. Good load capacity of anchor pile is the key factor to the guarantee of safe workover operation. The load capacity test of anchor pile is complete by connecting vibration test and method of mechanical impedance. The reduction coefficient must be used in calculating the anti-pulling load capacity because of difference of soil kinds. To testify the results from mechanical impedance method, the system of pulling pile directly is built. The average error of data from this system is within 5%. It can conclude that the method of mechanical impedance and vibration test can be popularized widely to load capacity of anchor pile, especially in different kinds of soil. The research can enrich the theories of uniform section pile and give the theoretical foundation to fix the anchor piles safely during workover rig operations.

FGF10 is a member of fibroblast growth factors (FGFs). We previously showed that FGF10 protects neuron against oxygen-glucose deprivation injury in vitro ; however, the effect of FGF10 in ischemic stroke in vivo is unknown. In the present study, we showed that FGF10 was mainly expressed in neurons but not astrocytes and detected FGF10 in mouse cerebrospinal fluid. The FGF10 levels in neurons culture medium and cell lysate were much higher than those in astrocytes. FGF10 expression in brain tissue and FGF10 level in CSF were increased in mouse middle cerebral artery occlusion (MCAO) model. Administration of FGF10 into lateral cerebroventricle not only decreased MCAO-induced brain infarct volume and neurological deficit, but also reduced the number of TUNEL-positive cells and activities of Caspases. Moreover, FGF10 treatment depressed the triggered inflammatory factors (TNF-α and IL-6) and NF-κB signaling pathway and increased phosphorylation of PI3K/Akt signaling pathway. Blockade of PI3K/Akt signaling pathway by wortmannin and Akt1/2-kinase inhibitor, partly compromised the neuroprotection of FGF10. However, blockade of PI3K/Akt signaling pathway did not impair the anti-inflammation action of FGF10. Collectively, our results demonstrate that neuron-derived FGF10 ameliorates cerebral ischemia injury via inhibiting NF-κB-dependent neuroinflammation and activating PI3K/Akt survival signaling pathway in mice.