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Copyright of Journal of Kunming Medical University / Kunming Yike Daxue Xuebao is the property of Kunming Medical Journal and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Interdisciplinary Studies of Literature is the property of Interdisciplinary Studies of Literature Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Electronic Components & Materials is the property of Electronic Components & Materials and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective:To investigate the correlation between single nucleotide polymorphisms (SNPs) of DC-DC2 (rs6456593, rs807701 and rs2274305) and KIAA0319 (rs4504469 and rs9461045) polymorphism interactions and developmental dyslexia. Methods: A total of 392 Uyghur children were enrolled in Xinjiang. Three SNPs (rs6456593, rs807701 and rs2274305) of DCDC2 and two SNPs (rs4504469 and rs9461045) of KIAA0319 polymorphisms were genotyped by SNPscan SNP typing. After Handy-Weinberg equilibrium (HWE) tests, the gene-gene interactions were detected by the Multifactor Dimensionality Reduction (MDR), and a logistic regression was employed to verify the best model. Results:Single-gene analysis showed that rs6456593 in genotype distribution (P<0.05), rs2274305 in allele frequency (P <0.05) and rs9461045 in both genotype distribution (P<0.05) and allele frequency (P <0.01) had significant differences between the cases and controls. With the rs6456593 and rs2274305 of DCDC2, and rs4504469 and rs9461045 of KIAA0319 combinations were judged as "high-risk" population by MDR (cross-validation consistency was 10/10, testing balance accuracy was 0.596), and other combinations were discriminated as the "low-risk" population. The risk of developmental dyslexia in "high-risk" population was 4.66 times as compared with the "low-risk" population OR =4. 66,95% CI: 3. 03 ~7.16), and the interaction was statistical significant (P = 0.021). Conclusion: There is interaction between SNPs of DCDC1 (rs6456593, rs807701 and rs2274305) and KIAA0319 (rs4504469 and rs9461045) polymorphism It may increase the risk of dyslexia in Xinjiang Uyghur children. [ABSTRACT FROM AUTHOR]

Copyright of Computer Engineering & Science / Jisuanji Gongcheng yu Kexue is the property of Computer Engineering & Science and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To study the feasibility of the establishment of the transplanted hepatoma rats model with abnormal savda syndrome and evaluate the intervention of Abnormal Savda Munziq (ASM). Methods: The rats were divided into the control group, the model control group, the model with the abnormal savda syndrome group and the treatment group with ASM(2.53, 5.06, 10.12 g/kg). The transplanted hepatoma rats model was established by inoculating walker-256 ascites tumor cells into the liver. The model rats with abnormal savda syndrome was first established by using multi-complicated induced methods for 3 weeks, such as electric shock, cold feeding environment and iron pipe braking, etc, then were inoculated the walker-256 ascites tumor cells into the liver. The treatment groups were administrated with the ASM 2.53, 5.06, 10.12 g/kg for two weeks after the rats model with abnormal savda syndrome has injected tumor cells. The tumor incidence, tumor size, the ascites formation rate and abdominal metastatic rate were calculated and the tumor cell morphological structure changes were observed under the light microscope and electron microscope. Results: Between the model control group and the model with the abnormal savda syndrome group, there were no statistical significance in the tumor incidence, abdominal metastatic rate and tumor size (P> 0.05), but compared with the model control group, the ascites formation rate was significantly higher in the model with the abnormal savda syndrome group (P< 0.05); Compared with the model with abnormal savda syndrome, there were obvious decrease of tumor size, the ascites formation rate and abdominal metastatic rate in the treatment group with ASM (2.53, 5.06 g/kg), and there was only significantly decrease of the ascites formation rate in 10.12 g/kg ASM. Under the light microscope and electron microscope, we found edema degree of tumor cell aggravated, necrosis tumor cells and infiltrated inflammatory cells increased in the groups of ASM. Conclusion: Abnormal savda may promote the formation of ascites and metastasis of liver cancer, then affect the development and outcome of liver carcinoma; ASM has a certain anti-cancer effect and improve tumor outcome through demaging tumor cells and reducing ascites and metastatic. [ABSTRACT FROM AUTHOR]

Copyright of Southwest China Journal of Agricultural Sciences is the property of Editorial Department of Southwest China Journal of Agricultural Sciences and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To study the expression of moleculars related to Rho/Rock signaling pathway in the transplanted hepatoma rats model with abnormal savda syndrome and explain the molecular biology mechanism of high incidence of abnormal savda syndrome tumors. Methods: The rats model with abnormal savda syndrome were developed by electric shock, cold feeding, iron pipe braking and other factors for 21 days. Then the transplanted hepatoma rats model were established by inoculating walker-256 ascites tumor cells into the liver. At last the changes of morphological structure was observed and the expression of related proteins was detected by Western Blot method in rats’ liver. Results: Compared with the control group, obvious tumor nests could be observed in the model with the abnormal savda syndrome group, the adjacent tissue of the cancer was disordered, the cancer cells migrated to the deep of hepatic lobule;Cancer cells disintegration and apoptosis、collagen proliferation、reconstruction of hepatic cord near cancer could be observed in the treatment group with ASM. Compared with the control group, the expression of Cdc42 and Rock2 proteins was significantly higher in the model control group(P<0.05), the expression of Cdc42, Rac1, Rock1, Rock2 and Myl1 proteins was significantly higher in the model with the abnormal savda syndrome group(P<0.05); Compared with the model with the abnormal savda syndrome group, the expression of Cdc42, Rac1, Rock1, Rock2 and Myl1 proteins showed dose-dependent decrease in the treatment group with ASM(P <0.05).Conclusion: There was certain correlation between the model with the abnormal savda syndrome and tumor cells invasion, transfer caused by moleculars related to Rho/Rock signaling pathway regulating actin contraction, ASM might reverse the injury of histomorphology through down-regulating the moleculars related to Rho/Rock signaling pathway. [ABSTRACT FROM AUTHOR]

Copyright of Computer Measurement & Control is the property of Magazine Agency of Computer Measurement & Control and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To study the expressione of autophagy-related protein Beclin-1 and LC3 in cortex and hippocampus of rats after cerebral ischemia reperfusion injury and the efficacy of Edaravone. Methods: Sprague Dawley rats were randomly divided into sham group,model group and Edaravone group. The cerebral ischemia reperfusion model was induced via Zea Longa with blocking the middle cerebral artery of 2 h and reperfusing of 24 h. Animals assigned to sham group were only separated left common carotid artery. Edaravone was injected intraperitoneally at a dose of 1 0 mg/kg at 15 min before reperfusion. The condition of nerve injury of rats was conducted by Neurobehavioral score. The degree of brain injury and success of model were determined based on 2, 3, 5-triphenyltetrazolium chloride(TTC)staining. The changes of neuron stained by hematoxylin and eosin (HE) in cortex and hippocampus were observed.The expression of Beclin-1 and LC3 was measured by immunohistochemistry. Results: After cerebral ischemia reperfusion the neurobehavioral score of edaravone group was(2.00± 0.67), which was obcviously less than(2.50± 0.53) of model group(P＜0.05). The infraction focus and the neuron injury in cortex and hippocampus neurons were also observed in model group, and the edaravone group reduced above expression. The positive rate of Beclin-1 of each group in cortex were (1 1.08± 0.85)％,(33.42± 1.57)％ and (25.61± 1.39)％, there was significant difference between model group with sham group and edaravone group (P＜0.05). The positive rate of Beclin-1 of each group in hippocampus were (10.34± 0.21)％,(31.82± 1.73)％ and (22.74± 1.26)％, there was significant difference between model group with sham group and edaravone group(P ＜ 0.05). The positive rate of LC3 of each group in cortex were (15.33± 0.47)％,(39.72± 1.73)％ and (28.53± 1.61)％, there was significant difference between model group with sham group and edaravone group(P＜0.05). The positive rate of LC3 of each group in hippocampus were (13.74± 0.37)％,(32.53± 1.43)％ and(25.38± 1.23)％, there was significant difference between model group with sham group and edaravone group (P＜0.05). Conclusion: The expression of Beclin-1 and LC3 was increased after cerebral ischemia reperfusion. Edaravone may reduce autophagy and brain injury through downregulation the expression of Beclin-1 and LC3. [ABSTRACT FROM AUTHOR]