The expression of Smad2 and Smad3 and the influence of exogenous transforming growth factorβ₁ (TGFβ₁) on them in rat bone marrow-derived mesenchymal stem cells (MSCs) cultured in vitro were investigated. The effects of different concentrations of TGFβ₁ on cell proliferation and ALP activity were detected by MTT and PNPP in, MSCs respectively. The expression of Smad2 and Smad3 and the influence of exogenous TGFβ₁ on them were also examined by immunocytochemistry and Western blot assays. The exogenous TGFβ₁ induced a dose-dependent decrease in cell proliferation and a dose-dependent increase, in ALP activity, which plateaued at 5 ng/ml. Smad2 and Smad3 proteins were detected only in the cytoplasm in the absence of TGFβ₁ and TGFβ₁ could stimulate the translocation of them from the cytoplasm to the nucleus. The total amount of Smad2 protein remained unchanged before and after TGFβ₁ treatment (P>0.05). The expression levels of Smad3 remained unchanged after 3 h and 6 h treatment (P>0.05), but decreased markedly after 24 h treatment (P<0.05). It was concluded that TGFβ₁ is a latent osteoinductive factor involved in osteoblastic differentiation. Both Samd2 and Samd3 mediate TGFβ₁ signaling as downstream mediators in MSCs. The biological output of TGFβ₁ triggering the osteoblastic differentiation could be entirely determined by Smad3 in MSCs.

The experience in diagnosis and treatment of bleeding complications in severe acute pancreatitis (SAP) by transcatheter arterial embolization was summarized. The clinical data of 19 SAP patients complicated with intra-abdominal bleeding in our hospital from Jan. 2000 to Jan. 2003 were analyzed retrospectively and the therapeutic outcome, of TAE was evaluated statistically. The results showed that the short-term successful rate of hemostasis by TAE was 89.5% (17/19), the incidence of re-bleeding after TAE was 36.8% (7/19) and the successful rate of hemostatis by second TAE was 71.4% (5/7). It was concluded that the intra-abdominal bleeding in SAP was mainly caused by the rupture of erosive/infected pseudoaneurysm. Mostly, the broken vessels were splenic artery and gastroduodenal artery. In terms of emergence hemostatis, TAE is the most effective method. Surgical hemostasis is necessary if hemostasis by TAE is failed or re-bleeding occurs after TAE.

In this study we tried to investigate the effect of fructose-1,6-diphosphate and HTK solution on protecting primary cardiac muscle cells of rat with cold preservation. The primary cardiac muscle cells of rat were cultured in vitro with four preservation solutions respectively: 0.9% sodium chloride solution (group A), FDP (group B), HTK solution (group C) and a mixture of FDP and HTK solution (group D). The cells were preserved for 6, 8 and 10 h at 0–4°C. The values of AST and LDH-L and the Na⁺-K⁺ ATPase activity in cardiac muscle cells were detected, and the survival rate of cardiac muscle cells was detected with trypan blue staining. The values of AST and LDH-L in group C and group D were remarkable lower those in group A and group B (P<0.001), while the Na⁺-K⁺ ATPase activity and the survival rate of cells in group C and group D were much higher than those in group A and group B (P<0.001). The values of AST and LDH-L after 6 hours in group D decreased much more than those in group C (P<0.01), while the Na⁺-K⁺ ATPase activity and the survival rate of cells in group D improved more than those in group C (P<0.01). Both of the HTK solution and the mixture of HTK and FDP solution have an evident effect on protecting the primary cardiac muscle cells of rat in vitro with cold preservation, Compared with the HTK solution, the mixture solution has a better short-term protective effect.

To study the effect of tumor necrosis factor-related apoptosis inducing ligand (TRAIL) on PC-3M cell line, PC-3M cell line was incubated with gradient concentrations of TRAIL for 4–24 h. Annixin-V fluorescence staining and TUNEL method were employed to detect the apoptosis of PC-3M cells. The morphology of apoptotic PC-3M cells was observed by electron microscopy. The relationship between TRAIL concentrations and the percentage of apoptotic cells was evaluated by flow cytometry. The proliferation inhibitory ratio was calculated by using MTT colorimetry. Our results showed that apoptosis of PC-3M cells could be induced by treatment with TRAIL for at most 4 h. The results of flow cytometry and MTT colorimetry demonstrated a time- and concentration-dependent relationship between cell apoptosis rate and TRAIL concentration. It is concluded that apoptosis of PC-3M cells can be induced by TRAIL. Because of the selective killing effect of TRAIL on tumor cells, it may become a potential alternative for the treatment of advanced prostate cancer.