Objective To observe the effect of the 8-word bandage on the walking ability of stroke patients with knee hyperextension. Methods Fifty patients with stroke combined with knee hyperextension were randomly divided into the observation group and the control group with 25 cases in each group. The control group was treated with conventional methods, including Bobath technology, Brunnstrom therapy and motor relearning primarily rehabilitation training. In addition to the conventional methods, patients in the observation group used 8-word bandage to fix knee joint in walking training. Before and after 8 weeks of treatment, Holden walking function classification, 10-meter maximum walking speed and improved Barthel index were adopted to evaluate the walking ability, maximum walking speed and the life ability of the patients. Results There were no significant differences in the scores before treatment between the two groups. The Holden walking function classification, the 10-meter maximum walking speed and the Barthel index scores were significantly improved after 8-week treatment in both two groups (P<0.05), and patient conditions were more significantly improved in the observation group than those of the control group (P<0.05). Conclusion Using 8-word bandage to fix knee joint can significantly improve knee hyperextension in patients with stroke, so as to improve the walking ability and activities of daily living.

Objective To investigate the role of interleukin-22 (IL-22)-regulated autophagy in hydrogen peroxide (H2 O2 )-induced hepatocarcinoma cell damage. Methods HepG2 cells were transfected with pEGFP-LC3 and then cultured in RPMI 1640 medium free of fetal bovine serum (FBS) or containing 1％ or 10％ FBS. These cells were pretreated with rapamycin or an autophagy inhibitor (3-MA) and then stimulated with recombinat human IL-22 (rhIL-22). GFP-LC3 puncta formation and autophagy signaling ac-tivation were measured. MTT assay was performed to detect cell viability. Results rhIL-22 significantly promoted GFP-LC3 puncta formation and LC3-Ⅱ expression in HepG2 cells treated with different stimulation protocols. The autophagy pathway inhibitor, 3-MA, dramatically suppressed the rhIL-22-activated autophagy signals. rhIL-22 attenuated H2 O2-mediated HepG2 cell death and that could be inhibited by 3-MA. Conclu-sion IL-22 promoted the activation of autophagy signaling pathways and alleviated H2 O2-mediated HepG2 cell damage.