Objective To evaluate the repairing effect of pedicle omentum on severe ureteral in-jury. Methods Twenty healthy dogs were randomized into the experiment group and the control group. Firstly the model of severe ureteral injury was made. In experimental group, the pedicle omen-turn were used to wrap up the severe injured ureter, but which was no done in control group. Urinary fistula and ureteral necrosis were observed. At 12 weeks postoperatively,the models were re-operated to investigate whether the severe injured ureters had healed. Angiogenesis, VEGF and its receptor KDR were also examined in stoma and surrounding tissue histopathologically. Results No urinary fistula was observed in experimental group, but 2 cases in control group were dead because of recurrent abdominal cavity infection after the formation of urinary fistula. The mucosa and smooth muscle of stoma were completely regenerated, and the blood vessels were regenerated more significantly in expe-rimental group than in the control group. In experimental group, the VEGF and KDR were over-ex-pressed, and the positive cell rates were (12. 65±0. 02)% and (10. 23±0. 03)%. But in control group, the stoma were not healed, and severe ureters1 strictures were observed in all dogs. Angiogene-sis was not signifieant, the VEGF and KDR positive cell rates were (1.54±0. 03)% and (2. 654± 0.04)%, respectively. Conelusions Pedicled omentum can promote the repair of severe ureteral in-jury. The mechanism may be the over expression of VEGF and KDR in prompting angiogenesis.

binding,cellular organelle membrane,and cellular metabolic process of GO enrichment.For the KEGG pathways, the target genes mainly concentrated on the focal adhesion pathway.Conclusion There is a different expression of novel microRNA between SLE and NC groups.The target genes from differently-expressed novel microRNA may play an important role in the pathogenesis of SLE and clinical symptoms and may be the unique target for further research.

Blood Glucose ; Humans ; Hydrocarbons, Brominated ; toxicity ; Occupational Exposure ; adverse effects

Heart failure with high prevalence is the endpoint of many cardiovascular diseases. Once diagnosed， patients usually need lifelong medication， which seriously affects their quality of life. The drugs commonly used to treat heart failure include angiotensin-converting enzyme inhibitors， beta-blockers， aldosterone receptor antagonists， and diuretics. However， the long-term use of those drugs can lead to side effects such as hypotension， depletion of body fluid， and electrolyte imbalance and even increase mortality. According to the theory of traditional Chinese medicine （TCM）， Qi deficiency and blood stagnation is the major cause of heart failure and when Qi is not moving， blood is not flowing. Therefore， the TCM clinical treatment of heart failure uses the Chinese medicinal materials which replenish Qi， activate blood， and dispell stasis to treat both internal cause and external symptoms. Recent studies have demonstrated that Chinese herbal medicines such as Astragali Radix， Ginseng Radix et Rhizoma， Notoginseng Radix et Rhizoma， Salviae Miltiorrhizae Radix et Rhizoma， Angelicae Sinensis Radix， as well as the compound formulas such as Buyang Huanwutang， Simiao Yongantang， Qili Qiangxin capsules， and Qishen Yiqi drops， play a significant role in the prevention and treatment of heart failure via replenishing Qi， activating blood， and dispelling stasis. Inhibition of oxidative stress and inflammatory responses， mitigation of myocardial fibrosis， improvement of calcium cycling， and protection of mitochondrial function represent the key mechanisms for the treatment of heart failure with Chinese medicinal materials. Focusing on the pathogenic mechanisms and signaling pathways of heart failure， this paper systematically describes the pharmacological effects， molecular mechanisms， and research progress in the clinical application of Chinese medicinal herbs with effects of replenishing Qi， activating blood， and dispelling stasis and their compound formulas in the prevention and treatment of heart failure， aiming to provide scientific evidence for the development and clinical use of anti-heart failure Chinese medicinal materials.

OBJECTIVETo investigate the expression of E2F1 gene in patients with acute leukemia(AL) and its clinical significance.

METHODSSeventy-two AL patients treated in March 2015 -March 2016 in our hospital were selected, and 24 healthy people were selected as controls. RT-PCR and Western blot were applied to determine the level of E2F1 gene transcription and expression, and the statistical analysis was performed to reveal the clinical value of E2F1 gene.

RESULTSThe relative expression levels of E2F1 gene and protein in bone marrow of AL patients was higher than that in control group (P<0.05). The levels of WBC, β-MG and LDH in the patients with high expression of E2F1 gene were higher than those in patients with low expression of E2F1 gene(P<0.05), but the E2F1 gene expression did not correlate with sex, fever, fatigue, bone marrow blast ratio, peripheral blood blasts ratio (P>0.05). The complete remission (CR) of patients with low expression of E2F1 was significantly higher than that of patients with high expression of E2F1(P<0.05). And the drug resistance in the patients with low expression of E2F1 gene was lower than that of patients with high expression of E2F1 gene (P<0.05). The expression level of E2F1 gene decreased significantly in patients with symptomatic remission after treatment (P<0.05). The expression levels of E2F1 gene in M1, M2 and M5 patients decreased significantly after treatment (P<0.05). Kaplan-Meier survival analysis showed that OS and DFS in the patients with low expression of E2F1 gene were higher than those in patients with high expression (P<0.05). Multivariate Cox regression analysis showed that the age and E2F1 gene were the independent influencing factors of OS (P<0.05); the sex and E2F1 gene were the dependent factors of DFS (P<0.05).

CONCLUSIONThe expression level of E2F1 gene in patients with AL has been found to be higher, the higher level of E2F1 gene closely relates with AL patients, E2F1 gene can be used as a biological target for the clinical treatment of AL.

Acute Disease ; Blood Cell Count ; Bone Marrow ; E2F1 Transcription Factor ; Humans ; Leukemia ; Prognosis ; Remission Induction

Objective To explore the protection and molecular mechanism of histone deacetylase inhibitors (HDACIs) on the spleen of rats with hemorrhagic shock. Methods A total of 60 SPF male SD rats were selected for the modeling of severe hemorrhagic shock using the method of arterial and venous cannulation with the time-divided bleeding. The measurement of mean arterial blood pressure and blood lactic acid was used to verify the modeling. The modeled rats were randomly divided into shock group, shock + suberoylanilide hydroxamic acid (SAHA) group, shock + autogenous transfusion group and shock + SAHA + autogenous transfusion group. Three hours after the treatment, the spleen of rats was collected and TUNEL method was employed to detect the apoptosis of spleen cells in each group. The statistical analysis was performed. Afterwards, real-time PCR and western blot were employed to detect the expression of BCL-2, BAX and caspass3 in the spleen of rats in each group. Results A total of 53 rats had successful modeling of severe hemorrhagic shock, with success rate of 88%. Cell apoptosis in the severe hemorrhagic model group was the most serious. After the intervention of HDACIs and the autogenous transfusion, the tissue injury was a bit recovered. Cell apoptosis was least in the shock + SAHA + autogenous transfusion group (P < 0.05). After the intervention of HDACIs and the autogenous transfusion, the relative expression of BCL-2 was significantly increased (P < 0.05), with highest relative expression of BCL-2 in shock + SAHA + autogenous transfusion group (P < 0.05). After the intervention of HDACIs and the autogenous transfusion, the relative expression of BAX was significantly decreased (P < 0.05), with lowest relative expression of BAX in the intervention group of single HDACIs. The change in the expression of caspass3 was similar to BAX, namely the relative expression of caspass3 was significantly decreased after the intervention of HDACIs and the autogenous transfusion (P < 0.05). Conclusions HDACIs and autogenous transfusion can all protect the spleen injury because of the severe hemorrhagic shock. Its molecular mechanism may be related to the regulation on the expression of BCL-2/BAX and caspass3, which may affect the apoptosis process of cells.