ABSTRACT
Mg3Sb2-based thermoelectric materials can convert heat and electricity into each other, making them a promising class of environmentally friendly materials. Further improving the electrical performance while effectively reducing the thermal conductivity is a crucial issue. In this paper, under the guidance of the oneness principle calculation, we designed a thermoelectric Zintl phase based on Mg3.2Sb1.5Bi0.5 doped with Tb and Er. Calculation results show that using Tb and Er as cationic site dopants effectively improves the electrical properties and reduces the lattice thermal conductivity. Experimental results confirmed the effectiveness of codoping and effectively enhanced thermoelectric performance. The most immense ZT value obtained by the Mg3.185Tb0.01Er0.005Sb1.5Bi0.5 sample was 1.71. In addition, the average Young's modulus of the Mg3.185Tb0.01Er0.005Sb1.5Bi0.5 sample is 51.85 GPa, and the Vickers hardness is 0.99 GPa. Under the same test environment, the material was subjected to 12 cycles in the temperature range of 323-723 K, and the average power factor error range was 1.8% to 2.1%, which is of practical significance for its application in actual device scenarios.
Subject(s)
Androgen-Insensitivity Syndrome/genetics , Mutation, Missense , Receptors, Androgen/genetics , Asian People , China , Homozygote , Humans , MaleABSTRACT
The posttranscriptional regulation of miRNAs is important for organism development. To investigate the role of miRNAs in angiogenesis, we performed a loss-of-function screening assay in human umbilical vein endothelial cells (HUVECs) and found that knockdown of 7 miRNAs (miR-95a, miR-126, miR-129, miR-137, miR-139, miR-200a, and miR-335) significantly suppressed cell viability. As miR-200a was highly expressed in HUVECs, blocking endogenous miR-200a using 2'-OMe antisense oligonucleotide (ASOs) resulted in a decrease of cell viability and migration. Bioinformatics analysis indicates the 3' untranslated region (UTR) of thrombospondin-1 (THBS1) has a putative binding site for miR-200a. MiR-200a can directly bind to THBS1 3'UTR and negatively regulate THBS1 expression. The identification of endothelial cells (ECs) related miRNA and its target gene may gain new insight into the mechanism of angiogenesis.
Subject(s)
Cell Movement/genetics , Cell Survival/genetics , Human Umbilical Vein Endothelial Cells/physiology , MicroRNAs/metabolism , 3' Untranslated Regions , Cells, Cultured , Gene Knockdown Techniques , Human Umbilical Vein Endothelial Cells/cytology , Humans , MicroRNAs/genetics , Neovascularization, Physiologic , Thrombospondin 1/genetics , Thrombospondin 1/metabolismABSTRACT
MicroRNAs (miRNAs) are short non-coding RNAs that negatively modulate gene expression at the post-transcriptional level and are known to be involved in the cross-talk between the host and virus. Using a standard plaque assay and real-time PCR method, we found that ectopic expression of miR-101 could significantly suppress herpes simplex virus-1 (HSV-1) replication, and that blocking endogenous miR-101 could increase viral progeny without affecting cell viability. Bioinformatics analysis indicates the 3' untranslated region (UTR) of mitochondrial ATP synthase subunit beta (ATP5B) has a putative binding site for miR-101. MiR-101 can directly bind to ATP5B 3'UTR and negatively regulate ATP5B expression. Using a RNA interference technique, knockdown of ATP5B significantly inhibited HSV-1 replication, indicating that ATP5B functions as a pro-viral factor. The ectopic expression of ATP5B lacking the 3'UTR could override the suppressive effect of miR-101 on HSV-1 replication. A concordant inverse correlation between miR-101 and ATP5B was observed in HSV-1-infected HeLa cells. Up-regulation of miR-101 expression may play a role in repressing productive HSV-1 replication by targeting ATP5B. Exploring the role of host-encoded miRNA in the regulation of viral infection would enable us to better understand the intricate networks of host-pathogen interactions.
Subject(s)
Herpesvirus 1, Human/immunology , MicroRNAs/metabolism , Mitochondrial Proton-Translocating ATPases/antagonists & inhibitors , Virus Replication/immunology , HeLa Cells , Herpesvirus 1, Human/physiology , Humans , MicroRNAs/genetics , Polymerase Chain Reaction , Viral Plaque AssayABSTRACT
Accumulating evidence suggests that microRNAs (miRNAs) control the replication of both RNA and DNA viruses. In order to determine whether host-encoded miRNAs affect hepatitis B virus (HBV) replication, antisense oligonucleotides (ASOs) of 328 identified human miRNAs were transfected into HepG2 2.2.15 cells, respectively. ELISA and MTS assay were used to measure the expression level of HBV S protein (HBsAg), HBV e antigen (HBeAg) and cell proliferation. Compared to experimental controls, miR-199a-3p and miR-210 efficiently reduced HBsAg expression without affecting HepG2 2.2.15 cell proliferation. Quantification of HBV DNA by real-time PCR showed that both miRNAs suppressed viral replication. Bioinformatics analysis indicated a putative binding site for miR-199a-3p in the HBsAg coding region and a putative binding site for miR-210 in the HBV pre-S1 region. The direct effect of miRNAs on the target region in HBV transcripts was validated by a fluorescent reporter assay, and the suppression of HBs gene expression by both miRNAs was measured by real-time PCR and Western blot. These results suggest that up-regulation of miR-199a-3p and miR-210 in HepG2 2.2.15 cells compared to HepG2 cells may play a role in regulating HBV replication and maintenance of a suitable level of virion production in persistent infection by targeting crucial HBV genes.
