Observations were made on 27 subjects suffering from burns. Treatment withexercise in water was given to 21 patients with 48--95%, or an average of 68.9%, ofthe body surface burned--37.3% of the affected area to cc 28.6% to deep Ⅱ?, and3% to superficial Ⅱ?. Six patients were in the control group, with 55--81%; or anaverage of 66.9%, of the body surface burned-36.5% of the affected area to Ⅲ?,26.7% to deep Ⅱ?, and 3.1% to superficial Ⅱ?, patients receiving this kind of treat-ment were required to do both active and passive exercises with the whole bodysubmerged in warm water before their wounds were completely healed. Then it wasfollowed by exercises on dry land. The control group did the same amount of exer-cise, but only on dry land. In terms of function recovery, 12 in the group under aquatic exercise treatmentgained "excellent" results and nine "good" results, while three in the controlgroup gained "satisfactory" results and the rest three showed no improvement. The advantages and efficacy of aquatic exercise treatment and precautions inusing this method were also discussed.

Background and Objectives: Epithelial-Mesenchymal transition (EMT) is one of the origins of myofibroblasts in renal interstitial fibrosis. Mesenchymal stem cells (MSCs) alleviating EMT has been proved, but the concrete mechanism is unclear. To explore the mechanism, serum-free MSCs conditioned medium (SF-MSCs-CM) was used to treat rat renal tubular epithelial cells (NRK-52E) fibrosis induced by transforming growth factor-β1 (TGF-β1) which ameliorated EMT. Methods: and Results: Galectin-3 knockdown (Gal-3 KD) and overexpression (Gal-3 OE) lentiviral vectors were established and transfected into NRK-52E. NRK-52E fibrosis model was induced by TGF-β1 and treated with the SF-MSCs-CM for 24 h after modelling. Fibrosis and autophagy related indexes were detected by western blot and immunocytochemistry. In model group, the expressions of α-smooth muscle actin (α-SMA), fibronectin (FN), Galectin-3, Snail, Kim-1, and the ratios of P-Akt/Akt, P-GSK3β/GSK3β, P-PI3K/PI3K, P-mTOR/mTOR, TIMP1/MMP9, and LC3B-II/I were obviously increased, and E-Cadherin (E-cad) and P62 decreased significantly compared with control group. SF-MSCs-CM showed an opposite trend after treatment compared with model group. Whether in Gal-3 KD or Gal-3 OE NRK-52E cells, SF-MSCs-CM also showed similar trends. However, the effects of anti-fibrosis and enhanced autophagy in Gal-3 KD cells were more obvious than those in Gal-3 OE cells. Conclusions SF-MSCs-CM probably alleviated the EMT via inhibiting Galectin-3/Akt/GSK3β/Snail pathway. Meanwhile, Gal-3 KD possibly enhanced autophagy via inhibiting Galectin-3/Akt/mTOR pathway, which synergistically ameliorated renal fibrosis. Targeting galectin-3 may be a potential target for the treatment of renal fibrosis.