Distal Actions of Automorphisms of Lie Groups G on Sub G

For a locally compact metrisable group G, we study the action of ${\rm Aut}(G)$ on ${\rm Sub}_G$ , the set of closed subgroups of G endowed with the Chabauty topology. Given an automorphism T of G, we relate the distality of the T-action on ${\rm Sub}_G$ with that of the T-action on G under a certain condition. If G is a connected Lie group, we characterise the distality of the T-action on ${\rm Sub}_G$ in terms of compactness of the closed subgroup generated by T in ${\rm Aut}(G)$ under certain conditions on the center of G or on T as follows: G has no compact central subgroup of positive dimension or T is unipotent or T is contained in the connected component of the identity in ${\rm Aut}(G)$ . Moreover, we also show that a connected Lie group G acts distally on ${\rm Sub}_G$ if and only if G is either compact or it is isomorphic to a direct product of a compact group and a vector group. All the results on the Lie groups mentioned above hold for the action on ${\rm Sub}^a_G$ , a subset of ${\rm Sub}_G$ consisting of closed abelian subgroups of G.

Harmonic Current Suppression of Dual Three-Phase PMSM Based on Model Predictive Direct Torque Control

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.

LncRNA H19 as a Competing Endogenous RNA to Regulate AQP Expression in the Intestinal Barrier of IBS-D Patients

ObjectiveThe study aimed to investigate the role of Long non-coding RNA (LncRNA) H19 in the pathogenesis of Diarrhea Irritable Bowel Syndrome (IBS-D), and further to the regulatory effect of LncRNA H19 on AQP1, 3 in the intestinal mucosa of IBS-D patients, so as to seek a new way to elucidate the mechanism of IBS in clinic.MethodsThe levels of LncRNA H19, AQP1, and AQP3 were detected in colonic tissues of IBS-D patients, compared with that in healthy controls. Through RNA gene interference and activation methods, small activating RNA (saRNA) and small interfering (siRNA) were transfered into Caco-2 cells in vitro experiment, and sub-group for two control group, siH19 empty vector group, siH19 interference group, overexpression H19 vector group, and overexpression H19 empty vector group. Quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot were applied to evaluate the expression levels of LncRNA H19 and the amount of AQP1 and AQP3 protein expression, respectively.ResultsCompared with healthy volunteers, the levels of LncRNA H19, AQP1, and AQP3 in the colonic mucosa of IBS-D patients were significantly decreased (P < 0.05). The results in vitro transfection experiment revealed that the level of LncRNA H19 in the siH19 interference group was significantly declined (P < 0.05), while there was a remarkable increase in the overexpression H19 vector group (P < 0.05), compared with the corresponding control groups. The expression of AQP1 and AQP3 in Caco-2 cells was of positive correlation with the level of LncRNA H19.ConclusionThat the down-regulation of LncRNA H19 resulted in the expression changes of AQP1 and AQP3 may play an important role in the occurrence and development of IBS-D.

PENGUKURAN PERBANDINGAN BELITAN PADA TRANSFORMATOR 3 PHASA 50 Hz 250 kVA

Transformator adalah peralatan listrik yang sangat vital dalam proses pembangkitan maupun transmisi energi listrik karena transformator dapat menaikan atau menurunkan tegangan yang diterima dari pembangkit listrik agar tegangannya disesuaikan dan bisa ditransmisikan sampai ke beban rumah tangga. Tap changer adalah alat yang berfungsi untuk mengubah perbandingan belitan transformator untuk mendapat tegangan operasi pada sisi sekunder sesuai yang dibutuhkan oleh tegangan jaringan (beban). Hasil Perbandingan belitan transformator bergantung pada vector group yang digunakan. Pengukuran perbandingan belitan dapat dilakukan dengan menggunakan alat Transformer Turn Ratio Test (TTR), dengan toleransi yang dijinkan 0,5 % dari rasio tegangan atau 1/10 dari persentase impedansi pada tapping nominal.

Expression of SASH1 in Preeclampsia and Its Effects on Human Trophoblast

Aim. To explore the involvement of SASH1 in preeclampsia. Methods. Expression of SASH1 was determined by qPCR, WB, and immunohistochemistry in the placenta of both normal and preeclamptic pregnancies. The SASH1 gene of human HTR-8/SVneo cells was overexpressed by transfection of pEZ-Lv206-SASH1. After that, the CCK-8 assay, EdU assay, transwell assay, and flow cytometry were used to examine the cell proliferation, migration, invasion, and apoptosis. Results. Higher expression of SASH1 was detected in placental tissues collected from patients with preeclampsia, compared with those from gestational age-matched control samples. The expression of SASH1 was significantly enhanced by transfection with pEZ-Lv206-SASH1 in HTR-8/SVneo cells. In addition, the HTR-8/SVneo cells transfected with pEZ-Lv206-SASH1 exhibited significantly reduced proliferation, migration, and invasion ability compared to the cells in the empty vector group and normal group. Flow cytometry analysis demonstrated that the apoptosis rate of cells transfected with pEZ-Lv206-SASH1 was significantly higher than that of cells transfected with empty vector and untreated cells. Conclusions. SASH1 is significantly upregulated in the placenta of preeclampsia, and overexpression of SASH1 can inhibit the proliferation, migration, and invasion, but induce apoptosis of trophoblast cells in vitro.

Lentiviral-Mediated Beclin-1 Overexpression Inhibits Cell Proliferation and Induces Autophagy of Human Esophageal Carcinoma Eca109 Cell Xenograft in Nude Mice

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.

Pdx1 expression up-regulated by Tet-on system induces the mouse embryonic stem cells to pancreatic-like cells through Notch pathway

Background The specific precursor cells derived from embryonic stem cells (ESCs) after induced differentiation offers great potential for repairing damaged pancreas. Therefore, it is of crucial importance to know whether pancreatic precursor cells with Pdx1+ could be induced to differentiate into pancreatic-like cells in vitro as well as the probable mechanism underlying. Methods In this study, mouse ESCs (ES-E14TG2a) were divided into the blank control group (ESC), the blank vector group (Pdx1− ESC), and the Pdx1 lentiviral vector group (Pdx1+ ESC). We constructed lentiviral vectors with overexpressed Pdx1 in Tet-on system and screened the stably transfected cell lines after transfection. CXCR4+ (C-X-C chemokine receptor type 4) DE cells of the three groups were seeded (day zero [d0]) after being sorted with immune beads, and expression of Pdx1 was induced on the second day (d1). Then, markers for the differentiation of Pdx1+ pancreatic precursor cells and molecules in the Notch pathway were detected at d3, d7, d10, and, d14. Results We found that expressions of Ptf1a, CK19, and amylase increased at d3 and d7, Neuro D1 increased at d10 and d14, Pax6 and insulin increased at d14, as well as Notch1, Notch2, Hes1, and Hes5 increased at d3 and thereafter declined at d14 in the Pdx1+ ESC group. These expressions were significantly higher than those in the ESC group and Pdx1− ESC group, but no marked differences were observed between the ESC group and Pdx1− ESC group. Conclusions Our study indicates that Pdx1+ pancreatic precursor cells can differentiate into pancreatic-like cells in which the Notch pathway plays important roles.

Poly(I:C) preconditioning ameliorates cognitive dysfunction after cerebral I/R injury by inhibiting TRAF6 signaling

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.