scholarly journals Campana points of bounded height on vector group compactifications

Author(s):  
Marta Pieropan ◽  
Arne Smeets ◽  
Sho Tanimoto ◽  
Anthony Várilly‐Alvarado
Keyword(s):  
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.


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.


2007 ◽  
Vol 59 (5) ◽  
pp. 917-942 ◽  
Author(s):  
Bradley N. Currey

AbstractGiven a semidirect product G = N ⋊ H where N is nilpotent, connected, simply connected and normal in G and where H is a vector group for which ad() is completely reducible and R-split, let τ denote the quasiregular representation of G in L2(N). An element ψ ∈ L2(N) is said to be admissible if the wavelet transform f ⟼ 〈 f, τ(·)ψ 〉 defines an isometry from L2(N) into L2(G). In this paper we give an explicit construction of admissible vectors in the case where G is not unimodular and the stabilizers in H of its action on are almost everywhere trivial. In this situation we prove orthogonality relations and we construct an explicit decomposition of L2(G) into G-invariant, multiplicity-free subspaces each of which is the image of a wavelet transform . We also show that, with the assumption of (almost-everywhere) trivial stabilizers, non-unimodularity is necessary for the existence of admissible vectors.


This paper is concerned with the restrictions that local symmetry requirements impose on the structures of model clusters chosen for the reproduction of electronic structure, as densities of states, in metals. Simple techniques for the identification of such local symmetries from wave vector group symmetries are outlined. The theory is applied to iridium and comparisons are made between the calculated and measured dialectric function related to the reflectivity of the metal.


2014 ◽  
Vol 998-999 ◽  
pp. 252-255
Author(s):  
Li Song Chen ◽  
Xiao Dong Gai ◽  
Chun Li

In order to explore the related mechanism of Foxp3 in tumor immune escape, the study detected the expression of Foxp3 in lewis lung cancer (LLC) cells and analyzed the expression of TGF-β1 and IL-10 in Foxp3 overexpressed LLC cells. Foxp3 mRNA was detected in LLC cells by RT-PCR. Foxp3 was highly expressed in Foxp3 transfected LLC group than that of in empty vector group and LLC group by RT-PCR(P <0.01). The mRNA and protein expression of TGF-β1 and IL-10 significantly increased in Foxp3 transfected LLC group than that of in empty vector group and LLC group by RT-PCR and ELISA(P <0.05). These results suggest that Foxp3 in LLC cells may promote tumor immune escape by enhancing the expression of TGF-β1 and IL-10.


2019 ◽  
Author(s):  
Meng She ◽  
Hao Feng ◽  
Zequn Feng ◽  
Gongming Wang ◽  
Guanghui Cheng ◽  
...  

Abstract To explore the role of PKCγ subunits of rostral anterior cingulate cortex (rACC) neurons in the development of bone cancer pain in rats. Healthy female Sprague-Dawley rats were randomly divided into five groups: blank control group (naive group), sham operation group (sham group), bone cancer pain group (BCP group), BCP plus empty lentiviral vector group (vehicle group) and BCP plus PKCγ/shRNA recombinant lentiviral vector group (PKCγ group). The BCP group, vehicle group and PKCγ group received a 10 µl intra-tibial injection of MADB-106 rat mammary carcinoma cell suspension (4.6×10 8 cell/ml). In comparison, the sham group received a 10 µl intra-tibial injection of saline. The mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were assessed on pre-operation day 0 (baseline) and days 3, 7, 14 and 21 after intra-tibial injection, respectively. To downregulate the PKCγ subunits of rACC neurons, the PKCγ group received a 10 µl bilateral rACC injection of shRNA/PKCγ recombinant lentivirus (1.25×10 9 TU/ml) on the day 7 after intra-tibial injection, whereas the vehicle group received an injection of the same dose of empty lentiviral vector. Western blotting, immunohistochemical and immunofluorescence analysis were performed to detect the different expression of PKCγ subunits in rACC neurons among these groups on postoperative days 7 or 21. No significant difference in the baseline of MWT and TWL was found among these five groups ( P > 0.05). However, compared with the naive group and sham group, the rats with bone cancer (BCP group, vehicle group and PKCγ group) demonstrated marked mechanical allodynia and thermal hyperalgesia that was evoked starting on postoperative day 7 following intra-tibial injection of carcinoma cells ( P < 0.05). Meanwhile, the western blotting analysis also confirmed that the expression of PKCγ in rACC neurons was significantly increased in the BCP model groups ( P < 0.05). However, from postoperative days 14-21, the injection of shRNA/PKCγ recombinant lentivirus in the PKCγ group alleviated mechanical allodynia and thermal hyperalgesia ( P < 0.05).The present study indicates that up-regulation of PKCγ subunits of rACC neurons in bone cancer pain rats contributes to the development of bone cancer pain.


2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Bicheng Lei ◽  
Lingwei Wu ◽  
Zhiming Lin ◽  
Pan Mei

The traditional direct torque control (DTC) method will produce a larger harmonic current in the x, y subspace when applied to a dual three-phase permanent magnet synchronous machine (DTP-PMSM) because the voltage vector used for DTC is not equal to zero in the x, y harmonic subspace. To mitigate this problem, in this manuscript, a model predictive direct torque control (MPDTC) method is proposed to eliminate the harmonic current in DTP-PMSM. The spatial distribution characteristic DTP-PMSM voltage vector is analyzed; then, the table of vector group can be obtained according to DTC, and each vector group can be combined to obtain the zero-voltage vector in the x, y subspace. According to the cost function, MPDTC selects the vector group and obtains the optimal vector sequence combination to eliminate the harmonic current in the x, y subspace. Furthermore, the MPDTC achieves closed-loop control of harmonic currents in the x, y subspace. The MPDTC can also eliminate harmonic currents caused by other factors. The simulation results show that the method of MPDTC can effectively suppress the harmonic current of DTP-PMSM.


Sign in / Sign up

Export Citation Format

Share Document