It is sometimes very difficult to extract a huge impacted stone through the T-tube fistulous tract by conventional techniques with choledochoscope. To simplify the procedure, a lithotriptor PSW-G type using plasma shock wave to disintegrate the stone was designed. The efficacy to fragmentate stone was investigated both in vitro and in vivo. Stones can be shattered into pieces less than 3 mm in diameter in about 30 times of spark with lower energy ranging from 1.7-3.4 kV and 1-3 J. Animal experiments were carried out to prove the safety of the lithotriptor. There was neither interference with the cardiovascular and respiratory systems nor obvious damage to the adjacent tissue where plasma shock wave applied to break stones. Six patients with retained calculi impacted both in extra- and intra-hepatic duct were successfully treated by plasma shock wave lithotripsy. It appears very useful in dealing with a huge impacted stone in the biliary tract.
This article presented the observation results of microcirculation of 84 island venous flaps performed on the ears of 42 rabbits. The survival rates of 5 groups divided by differently handling the vessel pedical of the flaps were: 1. maintaining artery and venous 90.36%. 2. maintaining distal and proximal venous 86.29%. 3. only maintaining proximal venous 75.71%. 4. only maintaining distal venous 28.75%. 5. ligating all vessels O(P < 0.01). The results of blood flow examined by laser Doppler and the number of micrangium counted by microcirculation microscope were decreasing upon the sequence of the above groups (P < 0.05). We found that there were exact microcirculation in the venous flaps of group 2, 3, 4, but the blood flow in these groups, especially the group 4, were slower than the group 1.
Abstract Osteosarcoma is the most common primary malignant tumor of bone, the long-term survival of which has stagnated in the past several decades. Celastrol, a triterpene from traditional Chinese medicine, has been proved to possess potent anti-tumor effect on various cancers. However, the effect of celastrol on human osteosarcoma and the underlying mechanisms remains to be elucidated. We reported here that celastrol could inhibit cell proliferation by causing G2/M phase arrest. Exposure to celastrol resulted in the activation of caspase-3, -8, and -9, indicating that celastrol induced apoptosis through both extrinsic and intrinsic pathways. Autophagy occurred in celastrol-treated cells as evidenced by formation of autophagosome and accumulation of LC3B-II. The celastrol-induced cell death was remarkably restored by the combination of autophagy and apoptosis inhibitors. Furthermore, inhibition of apoptosis enhanced autophagy while suppression of autophagy diminished apoptosis. Celastrol also induced JNK activation and ROS generation. The JNK inhibitor significantly attenuated celastrol-triggered apoptosis and autophagy while ROS scavenger could completely reverse them. The ROS scavenger also prevented G2/M phase arrest and phosphorylation of JNK. Importantly, we found that celastrol had the similar effects on primary osteosarcoma cells. Finally, in vivo , celastrol suppressed tumor growth in the mouse xenograft model. Taken together, our results revealed that celastrol caused G2/M phase arrest, induced apoptosis and autophagy via the ROS/JNK signaling pathway in human osteosarcoma cells. Celastrol is therefore a promising candidate for development of antitumor drugs targeting osteosarcoma.
Correction to: Cell Death and Disease (2014) 5, e1574. doi:10.1038/cddis.2014.535; published online 18 December 2014 Since the publication of this paper, it has been noted that the labelling WT and TLR4−/− was missing from the bottom of Figure 7g in the pdf file. The corrected article appears onlinetogether with this erratum.
This work aimed to explore the therapeutic effect of micropump intravenous infusion of ambroxol hydrochloride (AH) on respiratory distress syndrome (RDS) in premature infants.56 premature infants from 28 to 34 weeks were recruited for analysis in this work. According to the treatment methods, they were randomly divided into two groups, with 28 patients in each group. Patients in the experimental group were given intravenous AH by micropump, while those in the control group inhaled atomized AH. The therapeutic effects were evaluated by comparing the data after treatment.The results showed that the serum 8-iso-PGP2α level in the experimental group was 166.32 ± 49.52, which was substantially inferior to that in the control group (183.32 ± 52.54), p < 0.05. In the experimental group, PaO2, SaO2, and PaO2/FiO2 were 95.88 ± 12.82 mmHg, 95.86 ± 2.27%, and 346.81 ± 51.93 mmHg, respectively, after 7 days of treatment. Compared with the control group (88.21 ± 12.82 mmHg, 93.18 ± 3.13%, and 266.83 ± 48.09 mmHg), the difference was statistically significant, p < 0.05. The oxygen duration, respiratory distress relief time, and length of stay were 95.12 ± 12.53 h, 4.4 ± 0.6 d, and 19.84 ± 2.8 d, respectively, in the experimental group, while they were 145.92 ± 13.85 h, 6.9 ± 0.9 d, and 28.42 ± 3.7 d, respectively, in the control group, showing great differences (p < 0.05).Micropump infusion of AH in the treatment of premature RDS patients was more conducive to efficacy. It can alleviate the clinical symptoms of children with RDS, improve their blood gas indicators, relieve and repair the damage to alveolar epithelial cell lipids in children with RDS, and ultimately improve the therapeutic effect, which can be used for the clinical treatment of premature RDS.
Abstract The activation of Toll-like receptor 4 (TLR4) signaling has an important role in promoting lipid accumulation and pro-inflammatory effects in vascular smooth muscle cells (VSMCs), which facilitate atherosclerosis development and progression. Previous studies have demonstrated that excess lipid accumulation in VSMCs is due to an inhibition of the expression of ATP-binding cassette transporter A1 (ABCA1), an important molecular mediator of lipid efflux from VSMCs. However, the underlying molecular mechanisms of this process are unclear. The purpose of this study was to disclose the underlying molecular mechanisms of TLR4 signaling in regulating ABCA1 expression. Primary cultured VSMCs were stimulated with 50 μ g/ml oxidized low-density lipoprotein (oxLDL). We determined that enhancing TLR4 signaling using oxLDL significantly downregulated ABCA1 expression and induced lipid accumulation in VSMCs. However, TLR4 knockout significantly rescued oxLDL-induced ABCA1 downregulation and lipid accumulation. In addition, IL-1R-associated kinase 1 (IRAK1) was involved in the effects of TLR4 signaling on ABCA1 expression and lipid accumulation. Silencing IRAK1 expression using a specific siRNA reversed TLR4-induced ABCA1 downregulation and lipid accumulation in vitro . These results were further confirmed by our in vivo experiments. We determined that enhancing TLR4 signaling by administering a 12-week-long high-fat diet (HFD) to mice significantly increased IRAK1 expression, which downregulated ABCA1 expression and induced lipid accumulation. In addition, TLR4 knockout in vivo reversed the effects of the HFD on IRAK1 and ABCA1 expression, as well as on lipid accumulation. In conclusion, IRAK1 is involved in TLR4-mediated downregulation of ABCA1 expression and lipid accumulation in VSMCs.
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