Archisargoid flies (Diptera, Brachycera, Archisargidae and Kovalevisargidae) from the Jurassic Daohugou biota of China, and the related biostratigraphical correlation and geological age

<div><p>Nine impression fossils of archisargoid flies were examined, described here as eight species (seven new), in seven genera (two new): <i>Archirhagio mostovskii</i> sp. nov., <i>Archirhagio varius</i> sp. nov., <i>Mesosolva huabeiensis</i> (Hong, <a href="#cit0009" target="_blank">1983</a>), <i>Novisargus rarus</i> gen. et sp. nov., <i>Ovisargus</i> (<i>Ovisargus</i>) <i>singulus</i> sp. nov., <i>Sharasargus maculus</i> sp. nov., <i>Tabanisargus daohugouensis</i> gen. et sp. nov. (Archisargidae) and <i>Kovalevisargus haifanggouensis</i> sp. nov. (Kovalevisargidae). These findings suggest that archisargoid flies were already highly diverse in the Daohugou biota. Furthermore, there is a very close resemblance between the Daohugou and Karatau biotas, consistent with the numerous other genera of insects shared between the Daohugou and Karabastau formations. The geological age for the archisargoid-bearing non-marine volcano-sedimentary rocks is reassessed as latest Middle Jurassic (Callovian) – earliest Late Jurassic (Oxfordian) related to that of the Karabastau Formation, rather than Middle Jurassic Jiulongshan Formation or the Early Cretaceous Dabeigou and/or Yixian formations.</p><p><a href="http://zoobank.org/urn:lsid:zoobank.org" target="_blank">http://zoobank.org/urn:lsid:zoobank.org</a>:pub:6B735695-DE37-4933-B449-B5EDE7A8A73A</p></div

Additional file 1 of Evaluation of post-dilatation on longitudinal stent deformation and postprocedural stent malapposition in the left main artery by optical coherence tomography (OCT): an in vitro study

Supplementary Material

microRNA 126 Inhibits the Transition of Endothelial Progenitor Cells to Mesenchymal Cells via the PIK3R2-PI3K/Akt Signalling Pathway

<div><p>Aims</p><p>Endothelial progenitor cells (EPCs) are capable of proliferating and differentiating into mature endothelial cells, and they have been considered as potential candidates for coronary heart disease therapy. However, the transition of EPCs to mesenchymal cells is not fully understood. This study aimed to explore the role of microRNA 126 (miR-126) in the endothelial-to-mesenchymal transition (EndMT) induced by transforming growth factor beta 1 (TGFβ1). </p> <p>Methods and Results</p><p>EndMT of rat bone marrow-derived EPCs was induced by TGFβ1 (5 ng/mL) for 7 days. miR-126 expression was depressed in the process of EPC EndMT. The luciferase reporter assay showed that the PI3K regulatory subunit p85 beta (PIK3R2) was a direct target of miR-126 in EPCs. Overexpression of miR-126 by a lentiviral vector (lenti-miR-126) was found to downregulate the mRNA expression of mesenchymal cell markers (α-SMA, sm22-a, and myocardin) and to maintain the mRNA expression of progenitor cell markers (CD34, CD133). In the cellular process of EndMT, there was an increase in the protein expression of PIK3R2 and the nuclear transcription factors FoxO3 and Smad4; PI3K and phosphor-Akt expression decreased, a change that was reversed markedly by overexpression of miR-126. Furthermore, knockdown of PIK3R2 gene expression level showed reversed morphological changes of the EPCs treated with TGFβ1, thereby giving the evidence that PIK3R2 is the target gene of miR-126 during EndMT process. </p> <p>Conclusions</p><p>These results show that miR-126 targets <i>PIK3R2</i> to inhibit EPC EndMT and that this process involves regulation of the PI3K/Akt signalling pathway. miR-126 has the potential to be used as a biomarker for the early diagnosis of intimal hyperplasia in cardiovascular disease and can even be a therapeutic tool for treating cardiovascular diseases mediated by the EndMT process.</p> </div

miR-126 activated the PI3K/Akt and inhibited the FoxO3/Smad4 signalling pathways in TGFβ1-induced EPCs.

<p>After the treatment with TGFβ1 (5 ng/mL) for 7 days, the protein in EPCs were prepared. Immunoblotting assays were performed using specific antibodies against PI3K, phosphor-Akt, Akt, FoxO3, and Smad4. β-actin and lamin A were used as internal controls for total cells and the nuclear proteins assay separately. The relative protein levels of these proteins were determined by densitometry analysis (n = 3). Data are shown as mean ± S.D. values. * and ** represent P < 0.05 and P < 0.01 with an LSD t-test, respectively. The number of observations (n) represents the number of independent cell preparations. </p

miR-126 inhibits EPC EndMT via targeting PIK3R2.

<p>(A) PIK3R2 expression was down-regulated by PIK3R2siRNA. (B) After the pre-treatment with PIK3R2siRNA, EPCs were treated TGFβ1 (5 ng/mL) for 7 days to induce EndMT. The αSMA expressions were detected by using immunofluorescence staining (Bar=50 μM; Blue for DAPI; Red for αSMA). ** represents <i>P</i> < 0.01 with an LSD t-test.</p

TGFβ1-induced EPCs underwent EndMT.

<p>(A) Flow cytometry analysis showed that 95% of cells were positive for both CD34 and <i>KDR</i>. (B) After the treatment with TGFβ1 (5 ng/mL) for 7 days, the morphology changed in EPCs (original magnification ×200, Bar=200 μm). (C) The mRNA expression levels of endothelial cell markers (CD31 and vWF) and mesenchymal cell markers (α-SMA and myocardin) in TGFβ1-induced EPCs were determined by using qRT-PCR. (D) After the treatment with TGFβ1 (5 ng/mL) for 7 days, miR-126 expression in EPCs was determined by using qRT-PCR. EPCs without any treatment were used as the normal control. Data are shown as mean ± S.D. (n = 3). **, <i>P</i> < 0.01 compared with the normal control.. The number of observations (n) represents the number of independent cell preparations. </p

Overexpression of miR-126 inhibited the EndMT process of EPCs induced by TGFβ1.

<p>(A) The mRNA expression of progenitor cell markers (CD31, CD34, CD133, and <i>KDR</i>), (B) endothelial cell markers (VEGF, <i>Flt-1</i>, eNOS, and iNOS), and (C) mesenchymal cell markers (α-SMA, <i>sm22-α</i>, and myocardin) was determined by using qRT-PCR. (D) Protein expression of α-SMA was detected by immunofluorescence staining. EPCs induced by TGFβ1 were transfected with a miR-126-expressing lentiviral vector, an empty vector (lentivector), or neither, and EPCs without any treatment were used as the normal control. EPCs infected with an empty vector were used as the Lenti-miR control. Data shown are representative of 3 independent experiments. **, <i>P</i> < 0.01 compared with the Lenti-miR control. </p

PIK3R2 was a direct target of miR-126 in EPCs.

<p>(A) Diagram of <i>PIK3R2</i>-3′UTR-containing luciferase reporter gene construct and the 22-bp target site of miR-126 in <i>PIK3R2</i>-3′UTR. The mutated nucleotides in <i>PIK3R2</i>-3′UTR fragments are underlined. (B) Luciferase reporter assays. The wild-type or mutant reporter plasmids were cotransfected into EPCs, which were infected by control-lentivirus or miR-126-lentivirus. The relative luciferase values shown were normalized to transfections with the wild-type reporter plasmids. Values are the average ± S.D. of 3 replicates. (C)The scheme of the luciferase assay to evaluate the direct inhibition of mir-126 on PIK3R2 protein expression. (D) The expression levels of PIK3R2 mRNA in miR-126 EPCs, miR-126 control, and the negative control—all under TGFβ1 treatment—were examined by qRT-PCR. β-actin was used as an internal control. (E) The protein expression of PIK3R2 was examined by western blotting. β-actin was used as an internal control. ** represents <i>P</i> < 0.01 with an LSD t-test. </p

Comparison of trajectory tracking under different literatures.

Comparison of trajectory tracking under different literatures.</p

Fig 12 -

Trajectory of a square with an approximate 90° turning angle: (a) Reference trajectory; (b) Actual trajectory; (c) Comparison of the reference trajectory and the actual trajectory.</p