Objective To explore the role of chronic ethanol ingestion in pulmonary fibrosis. Methods Twenty SD rats were randomly divided into a control group (n=10) and an ethanol group ( n=10) , and fed with quantitative non-ethanol and ethanol Lieber-DeCarli liquid diet every day respectively. All rats were sacrificed after 8 weeks. The morphological changes and collagen deposition of lung tissue were observed under light microscope by HE and Masson staining. Levels of glutathione (GSH) and hydroxyproline (HYP) in lung tissues were measured by colorimetric method. The content of connective tissue growth factor (CTGF) in lung tissue was detected by ELISA. Results Compared with the control group, varied degrees of alveolar and alveolar septal infiltration of inflammatory cells can be shown in the ethanol group, and also some alveolar wall damage or collapse.Masson staining showed that the ethanol group has more significant deposition of collagen fibers in alveolar interstitumthan the control group. The content of GSH in rat lung tissue reduced, but the contents of HYP and CTGF increased in the ethanol group compared with the control group [ GSH( mg/g) :0.08±0.04 vs. 0.22±0.14, HYP(mg/g) : 0.57±0.15 vs. 0.40 ± 0.09, CTGF(ng/mL) :306.57±46.86 vs. 134.02±79.82, Plt;0.05] . Conclusions Lieber-DeCarli ethanol liquid diet can establish a rat model of chronic ethanol ingestion. Lung injury and pulmonary fibrosis in rats can be induced by chronic ethanol ingestion. Ethanol may be one of the causes of the pulmonary fibrosis.
【Abstract】ObjectiveTo investigate the efficacy of radiofrequency (RF) ablation comparing with percutaneous ethanol injection (PEI) in the treatment of postoperative recurrent hepatocellular carcinoma. MethodsOne hundred and thirtyseven patients with recurrent hepatocellular carcinoma excluding those with extrahepatic metastasis or Child C liver function were analyzed retrospectively. Of these patients, 74 cases with 86 lesions underwent RF therapy, while the other 63 cases with 75 lesions treated with PEI therapy. In RF group, the average size of lesions was 2.05 cm in diameter including 9 lesions were more than 3 cm in diameter (the maximum size of the lesions was 4 cm in diameter). In PEI group, all lesions were less than 3 cm in diameter, averagely 2.03 cm. Blood routine, liver function, AFP level and Doppler ultrasound were observed before and after therapy 1-year, 2-year, 3-year survival rates were calculated in two groups as well. Results①There was no serious complications in two groups. ②Complete tumor necrosis was 93.0%(80/86) in RF group and 81.3%(61/75) in PEI group. In RF group, complete tumor necrosis rate for lesions less than 3 cm in diameter was 96.1%(74/77), while that was only 66.7%(6/9) for lesions greater than 3 cm in diameter. ③The 1-year, 2-year, 3-year survival rates were 74.3%(55/74), 62.2%(46/74) and 54.8% (17/31) in RF group as well as 68.3%(43/63), 57.1%(36/63) and 45.0%(9/20) in PEI group， respectively. ④The average treatment needed to achieve tumor ablation were 1.3 for RF group, and 2.5 for PEI group，respectively. ConclusionRF is an efficient treatment for recurrent hepatocellular carcinoma.
The mechanisms of general anesthesia, which was introduced about 170 years ago, remain poorly understood. Even less well understood are the effects of general anesthesia on the human body. Recently we identified 18 G-protein coupled receptor (GPCR) genes of Daphnia pulex, an invertebrate model organism. Phylogenetic analysis identified these genes to be the homologs of the human γ-aminobutyric acid, type B (GABAB) receptor, metabotropic glutamate receptors (mGluR), adrenergic receptor, serotonin (5-HT) receptor, dopamine receptor and muscarinic acetylcholine receptor (mAChR). Using reverse transcription and quantitative PCR techniques, we systematically measured the effects of propofol, etomidate and ethanol on these 18 GPCR mRNA expressions in Daphnia pulex.
Objective To investigate the effect of chaiqin chengqi decoction (CQCQD) on serum lipid metabolism in experimental acute pancreatitis. Methods A total of 27 C57BL/6 mice were randomly divided into three groups (n=9 for each group). The mice in the acute pancreatitis model group (AP group) and the acute pancreatitis model + CQCQD treatment group (APQ group) received seven intraperitoneal injections of cerulein (50 µg/kg) at hourly intervals, while the mice in the control group (CON group) received phosphate-buffered saline injections at the same regimen of cerulein. Oral gavage of CQCQD (5.5 g/kg) or same volume of distilled water was commenced 1 h after the first cerulein injection for three times at intervals of 4 h for the APQ group and AP group, respectively. Animals were sacrificed 12 h after the first cerulein / phosphate-buffered saline injection for collecting serum and tissue samples. The levels of serum lipase and amylase, pancreatic histopathology assessment, as well as pancreatic myeloperoxidase activity, were used to assess the severity of acute pancreatitis and the efficacy of CQCQD. Additionally, serum lipid metabolites were analyzed in all groups. Results In comparison to the CON group, the mice in the AP group exhibited significant edema, inflammatory cell infiltration, necrosis of pancreatic tissues, as well as elevated levels of serum amylase, lipase, and pancreatic myeloperoxidase activity (P<0.05); in comparison to the AP group, inflammatory cell infiltration and necrosis of pancreatic tissue, as well as elevated level of serum amylase significantly reduced in the APQ group (P<0.05). A total of 319 lipid molecules were identified in serum, and 13 lipid metabolites were significantly increased in the AP group and successfully decreased in the APQ group, of which 9 were lyso-phosphatidylethanolamine (LPE) molecules involved in the glycerol phospholipid metabolic pathway. Further statistical analysis revealed that six of these LPE molecules could serve as potential biomarkers. Conclusions CQCQD ameliorated pancreatic injury and serum lipid metabolism disorder of acute pancreatitis model induced by cerulein and significantly improved the abnormal increase of serum LPE level. However, the role of LPE in acute pancreatitis and the underlying mechanisms of CQCQD on LPE metabolic pathways still need further study.