Antiferromagnetic phase transition in a 3D fermionic Hubbard model.

The fermionic Hubbard model (FHM)1 describes a wide range of physical phenomena resulting from strong electron-electron correlations, including conjectured mechanisms for unconventional superconductivity. Resolving its low-temperature physics is, however, challenging theoretically or numerically. Ultracold fermions in optical lattices2,3 provide a clean and well-controlled platform offering a path to simulate the FHM. Doping the antiferromagnetic ground state of a FHM simulator at half-filling is expected to yield various exotic phases, including stripe order4, pseudogap5, and d-wave superfluid6, offering valuable insights into high-temperature superconductivity7-9. Although the observation of antiferromagnetic correlations over short10 and extended distances11 has been obtained, the antiferromagnetic phase has yet to be realized as it requires sufficiently low temperatures in a large and uniform quantum simulator. Here we report the observation of the antiferromagnetic phase transition in a three-dimensional fermionic Hubbard system comprising lithium-6 atoms in a uniform optical lattice with approximately 800,000 sites. When the interaction strength, temperature and doping concentration are finely tuned to approach their respective critical values, a sharp increase in the spin structure factor is observed. These observations can be well described by a power-law divergence, with a critical exponent of 1.396 from the Heisenberg universality class12. At half-filling and with optimal interaction strength, the measured spin structure factor reaches 123(8), signifying the establishment of an antiferromagnetic phase. Our results provide opportunities for exploring the low-temperature phase diagram of the FHM.

Inhibitory effects of octreotide on the progression of hepatic fibrosis via the regulation of Bcl-2/Bax and PI3K/AKT signaling pathways.

In a previous study, we showed that octreotide alleviate hepatic fibrosis. However, its underlying molecular mechanisms are still poorly understood. In the current study, rats with CCl4-induced liver injury and Hepatic Stellate Cells (HSCs) were employed for in vitro and in vivo studies to observe the effects of octreotide on progression of liver fibrosis. The results in rats indicated that octreotide remarkably alleviated hepatic injury. The treated rats showed improved pathological manifestations and reduced liver indicators, e.g., liver weight, liver index and liver hydroxyproline (Hyp) content. Additionally, activities of serum total bilirubin (TBIL), aspartate transaminase (AST) and alanine transaminase (ALT), and serum levels of hyaluronic acid (HA), laminin (LN), type IV collagen (IV-C) and procollagen III peptide (PIIIP) also decreased. Furthermore, releasing inflammatory factors and proliferation of activated HSCs under different treatments were detected in which levels of IL-1ß, IL-6, TNF-α decreased and hepatocytes proliferative capacity reduced through Bcl-2/Bax-dependent apoptosis. Finally, our results demonstrated that octreotide was able to exert an inhibitory effect on the activation of HSCs regulating the PI3K/AKT signaling pathway. In summary, our study corroborated that octreotide could prevent liver fibrosis probably via modulating Bcl-2/Bax and PI3K/AKT signaling pathway.

Octreotide attenuates hepatic fibrosis and hepatic stellate cells proliferation and activation by inhibiting Wnt/ß-catenin signaling pathway, c-Myc and cyclin D1.

Fibrosis is the common results from an excessive wound-healing response to chronic liver injury. Otreotide (OCT), an analogue of somatostatin, was reported to have an anti-hepatic fibrosis effect. However, its anti-fibrosis mechanisms have not been well characterized to date. The present study aimed to investigate the protective effects of OCT on carbon tetrachloride (CCl4)-induced rat liver fibrosis and activation and proliferation of transforming growth factor-ß1 (TGF-ß1)-treated hepatic stellate cells (HSCs) and explore its anti-hepatofibrotic mechanisms. Our results indicated that treatment with OCT markedly down-regulated the protein and mRNA expression of liver fibrosis markers including α-smooth muscle actin (α-SMA) and collagen I in CCl4-induced rat model of liver fibrosis, accompanied by decreasing aspartate transaminase (AST), alanine transaminase (ALT), total bilirubin (TBIL) activities and increasing the serum level of albumin (ALB). In addition, in vitro results revealed that OCT inhibited the activation and proliferation of TGF-ß1-treated LX-2 cells in a concentration-dependent manner and decreased in parallel the expression of Wnt1, ß-catenin, c-Myc and cyclin D1, indicating that OCT might attenuate liver fibrosis, at least in part, by inhibiting Wnt/ß-catenin signaling pathway. Overall, these results provide a novel anti-fibrotic mechanism of OCT, which might be associated with its ability to repress Wnt/ß-catenin signaling pathway.