8 research outputs found

    Additional file 1 of Effects and mechanism of Aβ1−42 on EV-A71 replication

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    Additional file 1: Fig. S1. Aβ1–42 directly interacted with VP1 but not VP2. Vero cells were transfected with HA-VP1, HA-VP2, or pcDNA 3.1 + plasmid for 24 h and lysed with protein lysate containing phosphatase and protease inhibitor. Then, the lysis buffer supernatant was mixed with Aβ1–42 immobilized magnetic beads at 4 °C for 2 h. The bound beads were suspended with a 1 × sample loading buffer and boiled for 10 min. The binding of VP1 or VP2 was detected by WB assay with anti-HA antibod

    Ultrafine Nb<sub>2</sub>O<sub>5</sub> Nanocrystal Coating on Reduced Graphene Oxide as Anode Material for High Performance Sodium Ion Battery

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    Ultrafine niobium oxide nanocrystals/reduced graphene oxide (Nb<sub>2</sub>O<sub>5</sub> NCs/rGO) was demonstrated as a promising anode material for sodium ion battery with high rate performance and high cycle durability. Nb<sub>2</sub>O<sub>5</sub> NCs/rGO was synthesized by controllable hydrolysis of niobium ethoxide and followed by heat treatment at 450 °C in flowing forming gas. Transmission electron microscopy images showed that Nb<sub>2</sub>O<sub>5</sub> NCs with average particle size of 3 nm were uniformly deposited on rGO sheets and voids among Nb<sub>2</sub>O<sub>5</sub> NCs existed. The architecture of ultrafine Nb<sub>2</sub>O<sub>5</sub> NCs anchored on a highly conductive rGO network can not only enhance charge transfer and buffer the volume change during sodiation/desodiation process but also provide more active surface area for sodium ion storage, resulting in superior rate and cycle performance. <i>Ex situ</i> XPS analysis revealed that the sodium ion storage mechanism in Nb<sub>2</sub>O<sub>5</sub> could be accompanied by Nb<sup>5+</sup>/Nb<sup>4+</sup> redox reaction and the ultrafine Nb<sub>2</sub>O<sub>5</sub> NCs provide more surface area to accomplish the redox reaction

    Detection and identification of live tumor cells in a CSF sample.

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    <p>(A) The live tumor cells in the CSF sample of a patient with metastatic breast cancer were identified as TurboFP635<sup>+</sup>/CK<sup>+</sup>/DAPI<sup>+</sup> cells. (B) A live cancer cell cluster with heterogeneous expression of CK in the CSF sample was identified by VACV.</p

    Characterization of CTCs in blood samples detected with GLV-1h254.

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    <p>(<b>A</b>) The CTCs in mice bearing human PC-3 prostate cancer xenografts showed high-level expression of CD44, ALDH1, vimentin and N-cadherin. (<b>B</b>) The CTCs from the human metastatic breast cancer patient BC1 showed the strong expression of CD44. (<b>C</b>) The live CTCs in the human metastatic breast cancer patient BC5 showed the strong expression of ALDH1.</p

    Detection and identification of live human CTCs in blood samples.

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    <p>(A) VACV GLV-1h254 detected live CTCs in mice bearing human PC-3 prostate cancer xenografts. Infected CTCs were CK<sup>+</sup> (B) or EpCAM<sup>+</sup> (C). Live CTCs were also detected by GLV-1h254 in mice bearing human A549 non-small lung cancer xenografts (D). (E) The live CTCs in the patient BC1 were identified as TurboFP635<sup>+</sup>/EpCAM<sup>+</sup> or CK<sup>+</sup>/CD45<sup>−/</sup>DAPI<sup>+</sup> cells. (F) The live CTCs detected in the patient BC5 were confirmed to express EpCAM, PR, or HER2/neu markers. (G) The live CTCs in the patient BC7 were confirmed as TurboFP635<sup>+</sup>/CK<sup>+</sup>/DAPI<sup>+</sup> cells. (H) The live CTCs in the patient CC1 with metastatic colorectal cancer were identified as TurboFP635<sup>+</sup>/EpCAM<sup>+</sup> or CK<sup>+</sup>/CD45<sup>−/</sup>DAPI<sup>+</sup> cells. (I) The live CTCs in the metastatic lung cancer patient LC1 were confirmed as TurboFP635<sup>+</sup>/EpCAM<sup>+</sup>/DAPI<sup>+</sup> cells. (J) The VACV detected live CTCs in the metastatic melanoma patient MM1 were shown to express melanoma tumor markers Melan-A or microphthalmia-associated transcription factor.</p

    Prevention and therapy of CTCs in mice bearing human prostate cancer.

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    <p>(A) GLV-1h68 early treatment prevented CTC formation in the majority of mice (7/8) while mice in the PBS group showed an increase in CTC numbers. (B) GLV-1h68 late treatment resulted in a dramatic decrease in CTC numbers while CTC numbers in the PBS group increased greatly, and then fluctuated over time. (C) Almost all CTCs detected in the GLV-1h68 late treatment group were GFP-positive (infected) at two weeks after treatment. (D) Primary tumors regressed after GLV-1h68 early or late treatment. (E) Both GLV-1h68 early and late treatments significantly prolonged mouse survival (p = 0.002, GLV-1h68 early vs. PBS; p = 0.006 GLV-1h68 late vs. PBS).</p

    Supplementary Material for: Thrombolysis for acute wake-up and unclear onset strokes with alteplase at 0.6 mg/kg in clinical practice: THAWS2 Study

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    Introduction: The aim of this study was to determine the safety and efficacy of intravenous (IV) alteplase at 0.6 mg/kg for patients with acute wake-up or unclear onset strokes in clinical practice. Methods: This multicenter observational study enrolled acute ischemic stroke patients with last-known-well time >4.5 h who had mismatch between DWI and FLAIR and were treated with IV alteplase. The safety outcomes were symptomatic intracranial hemorrhage (sICH) after thrombolysis, all-cause deaths and all adverse events. The efficacy outcomes were favorable outcome defined as an mRS score of 0–1 or recovery to the same mRS score as the premorbid score, complete independence defined as an mRS score of 0–1 at 90 days, and change in NIHSS at 24 h from baseline. Results: Sixty-six patients (35 females; mean age, 74±11 years; premorbid complete independence, 54 [82%]; median NIHSS on admission, 11) were enrolled at 15 hospitals. Two patients (3%) had sICH. Median NIHSS changed from 11 (IQR, 6.75–16.25) at baseline to 5 (3–12.25) at 24 h after alteplase initiation (change, –4.8±8.1). At discharge, 31 patients (47%) had favorable outcome and 29 (44%) had complete independence. None died within 90 days. Twenty-three (35%) also underwent mechanical thrombectomy (no sICH, NIHSS change of –8.5±7.3), of whom 11 (48%) were completely independent at discharge. Conclusions: In real-world clinical practice, IV alteplase for unclear onset stroke patients with DWI-FLAIR mismatch provided safe and efficacious outcomes comparable to those in previous trials. Additional mechanical thrombectomy was performed safely in them
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