[Therapeutic strategies, practice, and prospect of a clinical cure for chronic hepatitis B in China].

Clinical cure (herein referred to as functional cure) is currently recognized as the ideal therapeutic goal by the guidelines for the prevention and treatment of chronic hepatitis B (CHB) at home and abroad. China has achieved significant results in research and exploration based on pegylated interferon alpha therapeutic strategies to promote the effectiveness of CHB clinical cure rates in clinical practice. The summary and optimization of clinical cure strategies in different clinical type classifications, as well as the exploration of clinical cure continuity and long-term outcomes, are of great significance for solving the current bottleneck problem and our future efforts in the developmental directions of clinical cure in CHB populations.

Rectification of swimming bacteria and self-driven particle systems by arrays of asymmetric barriers.

We show that the recent experimental observation of the rectification of swimming bacteria in a system with an array of asymmetric barriers occurs due to the ballistic component of the bacteria trajectories introduced by the bacterial "motor." Each bacterium selects a random direction for motion and then moves in this direction for a fixed period of time before randomly changing its orientation and moving in a new direction. In the limit where the bacteria undergo only Brownian motion on the size scale of the barriers, rectification does not occur. We examine the effects of steric interactions between the bacteria and observe a clogging effect upon increasing the bacteria density.

Effect of matrine on lipopolysaccharides/D-galactosamine-induced hepatitis and tumor necrosis factor release from macrophages in vitro.

AIM: To study the effects of matrine (Mat) on lipopolysaccharides (LPS)-induced fatal hepatitis in D-galactosamine (D-GalN)-sensitized mice and tumor necrosis factor (TNF) release from peritoneal macrophages (PMO). METHODS: Mice were pretreated with Mat (10, 50 mg.kg-1, i.p., bid x 3 d), and then injected i.p. LPS + D-GalN. Liver injury was assessed by quantifying plasma activity of alanine aminotransferase (ALT) and histopathological examination. The TNF activities in the supernatants of mouse PMO stimulated with LPS in the presence of Mat (32.5-500 mg.L-1) were monitored by the L929 target cells lytic assay. RESULTS: Mat pretreatment markedly diminished hepatic injury induced by LPS in combination with D-GalN. Mat inhibited LPS-induced TNF release from mouse PMO in vitro in a concentration-dependent manner. CONCLUSION: Mat protected the D-GalN-treated mice from the development of fatal hepatitis induced by LPS, and inhibited the LPS-induced TNF release from mouse PMO.

[Effect of matrine on mouse hepatitis and tumor necrosis factor production induced by Propionibacterium acnes/lipopolysaccharides].

The effect of matrine (Mat) on lipopolysaccharides (LPS)-induced fatal hepatitis and tumor necrosis factor (TNF) production in Propionibacterium acnes (PA)-primed mice were studied. Mice were injected i.p. LPS (10 micrograms/mouse) 7 d after i.p. PA (0.5 ml/mouse) to induce fatal hepatitis. After i.p. LPS, serum TNF activity rose to 1657 +/- 406 kU.L-1 at 1.5 h and ALT activity increased up to 1,496 +/- 890 U.L-1 at 5 h. Six of 8 mice died within 5 h and the massive hemorrhagic necrosis of the liver was observed in all mice. Administration of Mat (10, 50 mg.kg-1, i.p., bid x 3 d) before the LPS injection markedly reduced the elevation of serum TNF and ALT activity in a dose-dependent manner, and diminished the mortality induced by LPS. Liver congestion and necrosis induced by LPS in PA-primed mice were ameliorated markedly by Mat pretreatment. Mat (62.5-250 mg.L-1) inhibited LPS-induced TNF release from PA-primed mouse peritoneal macrophage in vitro in a concentration-dependent manner. These results seggest that Mat protected PA-primed mice from the development of fatal hepatitis induced by LPS due to inhibition of TNF production.