A local global principle for the elementary unimodular vector group

Author(s):  
Selby Jose ◽  
Ravi A. Rao
2020 ◽  
Vol 15 (1) ◽  
pp. 70-77
Author(s):  
Junhe Zhang ◽  
Weihua Dong

Background: Esophageal carcinoma is one of the common malignant tumors in digestive tract. BECLIN-1 is a key gene that regulates autophagy, and its abnormal expression may be related with many human tumors. However, the mechanism of BECLIN-1 in esophageal carcinoma remains unknown. Objective: In this study, we explored the effect of BECLIN-1 overexpression on tumor growth in mice with esophageal carcinoma and its mechanism. Methods: Recombined lentiviral vector containing BECLIN-1 was used to transfect human esophageal carcinoma Eca109 cells and establish stable cell line. qRT-PCR was used to detect BECLIN-1 mRNA level in the transfected Eca109 cells, CCK-8 assay was used to detect cell proliferation. Beclin-1, P62 and LC3-II protein expression levels in Eca109 cells were detected using Western blot analysis. Subcutaneous xenograft nude mice model of human esophageal carcinoma was established, and the tumor growths in Beclin-1 group, control group and empty vector group were monitored. Beclin-1 protein expression in vivo was detected by immunohistochemistry. Results: Beclin-1 mRNA and protein were overexpressed in Eca109 cells. Compared with empty vector group, the growth rate of cells transfected with BECLIN-1 decreased significantly. Compared with the control group and empty vector group, the expression level of P62 protein in beclin-1 group was significantly decreased, while the expression level of LC3-II protein was significantly increased. The tumor growth rate in nude mice of Beclin-1 group was significantly lower than that of the control group and empty vector group, and Beclin-1 protein was mainly expressed in Beclin-1 group in vivo. Conclusion: BECLIN-1 can induce autophagy in esophageal carcinoma Eca109 cells, and it can significantly inhibit the growth of esophageal carcinoma.


2016 ◽  
Vol 5 (04) ◽  
pp. 4974
Author(s):  
Ayoh Stephen O. ◽  
Olanrewaju Comfort A*

Ticks transmit a greater variety of pathogenic micro-organisms than any other arthropod vector group, and are among the most important vectors of diseases affecting animals. A survey on the prevalence of tick species infesting domestic birds sold in Gwagwalada main market, Abuja between April and July, 2015. A total of 450 birds were examined by feather separation with fingers and a pair of forceps to expose the skin of the birds for presence of the ticks. An overall prevalence of 25.6% was observed. Out of the 150 domestic fowls examined 62(53.9%) were infested, 44(29.3%) of the 150 Guinea fowl and 9(6.0%) of the 150 Pigeons were infested. Of all the ticks identified, 93(51.4%) were from the Domestic Fowls and 77(42.5%) from the Guinea fowl and 11(6.0%) from Pigeon. Thirty (32.3%) of the ticks from the Domestic fowls were Argas persicus, 25(26.9%) Argas walkerae, 20 (21.5%) Ornithodorus moubata and 18(19.4%) Ornithodorus savignyi. Similarly, 34(44.2%) of the ticks from Guinea fowl were A. walkerae, 20(28.2%) O. moubataand 23(32.4%) O. savignyi. Five (45.5%) of the ticks from Pigeon were A. persicus, 4 (36.4%) were A. walkerae, 2 (18.2%) were O. moubata and no O. savignyi. Observation on the location of tick from the hosts body showed highest prevalence was found under the wings (55.2%) and lowest on the head & neck (5.00%). The result of this research revealed that Gwagwalada market poultry section is endemic of tick infestation. Chemical control with acaricides and improved management and sanitation of the poultry cages in the market should be enforced.


2004 ◽  
Vol 141 (1) ◽  
pp. 369-379
Author(s):  
Peter Roquette

2014 ◽  
Vol 26 (1) ◽  
pp. 1-16 ◽  
Author(s):  
William D. Banks ◽  
Ahmet M. Güloğlu ◽  
Robert C. Vaughan

2020 ◽  
Author(s):  
Peng-Fei Wang ◽  
Wei-Bin Zhong ◽  
Xiao-Hua Ju ◽  
Zhen-Guang LI ◽  
Fa-Xiang Wang

Abstract Objective: Toll-like receptor (TLR) activation plays an important role in cerebral ischemia-reperfusion injury. In addition, increasing evidence suggests that TLRs may affect cognitive behavior through TLR-mediated signaling. Here, we explored the protective effects of TLR3 on cognitive dysfunction after ischemia in the context of poly(I:C) preconditioning.Materials and Methods : Mice (n=84) were randomly divided into the sham group, AAV (vector) group, middle cerebral artery occlusion (MCAO) model group, poly(I:C) (pre) + MCAO model group, and AAV (TRAF6) + poly(I:C) (pre) + MCAO model group. The mice were injected i.p. with poly(I:C) (1.25 mg/g) 24 h prior to cerebral ischemia. Then, neurological scores were assessed, and the infarct volume was measured after cerebral ischemia-reperfusion. We evaluated the poly(I:C) preconditioning-induced attenuation of neuronal damage using Nissl and TUNEL staining. We assessed the poly(I:C) preconditioning-mediated inhibition of I/R-induced glial activation, inflammatory factor levels and TRAF6 expression. We also assessed whether TRAF6 affects poly(I:C) preconditioning to improve cognitive dysfunction and neuroprotection.Results: The results showed that compared with those of the sham group and AAV (vector) group, the functional neurological scores and focal infarct volume of the MCAO group and poly(I:C) preconditioning group were significantly increased. The results also showed that compared with those of the MCAO group, the functional neurological scores and focal infarct volume of the poly(I:C) preconditioning group were significantly reduced. Our results indicated that poly(I:C) preconditioning significantly attenuated neuronal apoptosis and cell loss. Poly(I:C) preconditioning also inhibited I/R-induced glial cell activation and reduced NF-κB, TNF-α and IL-β levels. Our findings showed that poly(I:C) preconditioning affected cognitive dysfunction following cerebral I/R. Here, we observed that poly(I:C) preconditioning affected the expression and distribution of TRAF6 following cerebral I/R. TRAF6 overexpression abolished poly(I:C)-induced neuroprotection and worsened cognitive dysfunction in cerebral I/R injury.Significance: Our findings suggested that poly(I:C) preconditioning ameliorates cognitive dysfunction after cerebral I/R injury by inhibiting TRAF6 signaling, which is a potential therapeutic target for the treatment of cognitive dysfunction after stroke.


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