The pathogenesis and regulatory role of HIF-1 in rheumatoid arthritis.

Rheumatoid arthritis (RA) is a prevalent autoimmune disease that involves the overgrowth and inflammation of synovial tissue, leading to the degeneration and impairment of joints. In recent years, numerous studies have shown a close relationship between the hypoxic microenvironment in joints and the occurrence and progression of RA. The main cause of the pathological changes in RA is widely believed to be the abnormal expression of hypoxia-inducible factor-1 (HIF-1) in joints. This paper describes and illustrates the structure and primary functions of HIF-1 and explains the main regulatory methods of HIF-1, including the PHDs/HIF-1 α/pVHL pathway, factor-inhibiting HIF (FIH), regulation of inflammatory cytokines, and the NF-κB pathway. Furthermore, this paper discusses the mechanism of HIF-1 and its impact on inflammation, angiogenesis, and cartilage destruction in greater detail. We summarize previous research findings on the mechanism of HIF-1 and propose new potential treatments for RA based on the pathogenesis of HIF-1 in RA.

Large lateral shift near pseudo-Brewster angle on reflection from a weakly absorbing double negative medium.

We focus on the lateral shift for an electromagnetic wave reflected from a weakly absorbing double negative medium (DNM). A large lateral shift near the pseudo-Brewster angle is found, which may be negative or positive. We give an analytic expression for such a kind of lateral shift, from which the critical transition point for sign-changing of the lateral shift can be easily obtained. Theoretical analysis shows that the absorption of DNM, even though very weak, plays an important role in determining the lateral shift. As evidences, we calculate the lateral shift by means of the momentum method and perform the finite-difference time-domain (FDTD) simulations. We find that the results of our theoretical analysis are reliable.