Equivalent circuit of the Battery/Supercapacitor HESS in Boost mode.

<p>Equivalent circuit of the Battery/Supercapacitor HESS in Boost mode.</p

Adaptive fractional order sliding mode control for Boost converter in the Battery/Supercapacitor HESS - Fig 3

<p><b>Simulation results of the FASMC and ASMC strategy for the Battery/supercapacitor HESS:</b> (a) The turn-on voltage of the FASMC; (b) The inductor current of the FASMC; (c)The turn-on voltage of the ASMC; (d) The inductor current of the ASMC.</p

Specifications of equivalent circuit of the Battery/Supercapacitor HESS in Boost mode.

<p>Specifications of equivalent circuit of the Battery/Supercapacitor HESS in Boost mode.</p

Simulated output voltage responses due to the different λ by AFSMC.

<p>Simulated output voltage responses due to the different λ by AFSMC.</p

High-performance fractional order terminal sliding mode control strategy for DC-DC Buck converter

<div><p>This paper presents an adaption of the fractional order terminal sliding mode control (AFTSMC) strategy for DC-DC Buck converter. The following strategy aims to design a novel nonlinear sliding surface function, with a double closed-loop structure of voltage and current. This strategy is a fusion of two characteristics: terminal sliding mode control (TSMC) and fractional order calculation (FOC). In addition, the influence of “the controller parameters” on the “performance of double closed-loop system” is investigated. It is observed that the value of terminal power has to be chosen to make a compromise between start-up and transient response of the converter. Therefore the AFTSMC strategy chooses the value of the terminal power adaptively, and this strategy can lead to the appropriate number of fractional order as well. Furthermore, through the fractional order analysis, the system can reach the sliding mode surface in a finite time. And the theoretical considerations are verified by numerical simulation. The performance of the AFTSMC and TSMC strategies is tested by computer simulations. And the comparison simulation results show that the AFTSMC exhibits a considerable improvement in terms of a faster output voltage response during load changes. Moreover, AFTSMC obtains a faster dynamical response, smaller steady-state error rate and lower overshoot.</p></div

NAC treatment decreases myeloid differentiation of <i>Ptpn11</i> GOF mutant cells.

<p>(A) Bone marrow cells freshly harvested from five-month-old <i>Ptpn11^D61G/+</i> and <i>Ptpn11^+/+</i> mice (n = 5/group) were cultured in IL-3 (2 ng/ml) containing RPMI 1640 medium with or without N-Acetyl-Cysteine (NAC) (500 µM). After 7 days of culture, intracellular ROS levels were quantified by FACS as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0063152#pone-0063152-g001" target="_blank">Figure 1</a>. (B) Bone marrow cells freshly harvested from five-month-old <i>Ptpn11^D61G/+</i> and <i>Ptpn11^+/+</i> mice (n = 5/group) were assayed for colony forming units (CFUs) in 0.9% methylcellulose IMDM medium containing IL-3 (2 ng/ml) with or without NAC (500 µM). Hematopoietic cell colonies (CFU-GM) were counted and normalized. (C) Bone marrow cells freshly harvested from five-month-old <i>Ptpn11^D61G/+</i> and <i>Ptpn11^+/+</i> mice (n = 5/group) were immunostained with cell surface markers. Lineage⁻Sca-1⁺c-Kit⁺ (LSK) cells were sorted by FACS. Purified LSK cells were cultured in IL-3 (0.5 ng/ml) containing RPMI 1640 medium. NAC (500 µM) was added every other day. After 7 days of culture, percentages of myeloid (Mac-1⁺/Gr-1⁺) cells derived from the sorted LSK cells were assessed by FACS analysis (n = 5 per group).</p

Cellular ROS levels are increased in bone marrow cells of <i>Ptpn11 GOF</i> mutant mice.

<p>(A) Bone marrow cells freshly harvested from five-month-old <i>Ptpn11^D61G/+</i> and <i>Ptpn11^+/+</i> mice (n = 5/group) were loaded with 2′-7′-dichlorofluorescein diacetate (DCF-DA). In addition, bone marrow cells were treated with H₂O₂ (200 µM). Intracellular ROS levels were quantified by FACS. (B) Four-week-old <i>Ptpn11^{E76K neo/+}/Mx1-Cre+</i> and <i>Ptpn11^+/+/Mx1-Cre+</i> mice were treated by intraperitoneal injection of a total of 5 doses of polyinosine-polycyticyclic acid (pI-pC) (250 µg/mouse) administered every other day over 10 days as we previously described <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0063152#pone.0063152-Xu3" target="_blank">[29]</a>. Twelve weeks after pI-pC treatment, bone marrow cells were harvested from <i>Ptpn11^E76K/+</i> and <i>Ptpn11^+/+</i> mice (n = 5/group). Intracellular ROS levels were quantified by FACS as above.</p

Additional file 1 of Exploration of neuron heterogeneity in human heart failure with dilated cardiomyopathy through single-cell RNA sequencing analysis

Supplementary Material

ROS levels are increased in the myeloid cells but not in early stem/progenitor cells of <i>Ptpn11 GOF</i> mutant mice.

<p>(A) Bone marrow cells freshly harvested from five-month-old <i>Ptpn11^D61G/+</i> and <i>Ptpn11^+/+</i> mice (n = 5/group) were immunostained with cell surface markers. Stained cells were loaded with DCF-DA. Intracellular ROS levels in the gated LSK (Lineage⁻Sca-1⁺c-Kit⁺) cell population were quantified by FACS. (B) Bone marrow cells freshly harvested from five-month-old <i>Ptpn11^D61G/+</i> and <i>Ptpn11^+/+</i> mice (n = 5/group) were immunostained with cell surface markers. CMP (Lineage⁻c-Kit⁺Sca-1⁻CD16/32^medCD34⁺), GMP (Lineage⁻c-Kit⁺Sca-1⁻CD16/32^highCD34⁺), and MEP (Lineage⁻c-Kit⁺Sca-1⁻CD16/32^med/lowCD34⁻) cells were sorted by multi parameter FACS. Purified cells were then loaded with DCF-DA. Intracellular ROS levels in these cells were quantified by FACS. (C) Bone marrow cells freshly harvested from five-month-old <i>Ptpn11^D61G/+</i> and <i>Ptpn11^+/+</i> mice (n = 5/group) were immunostained with Mac-1 and Gr-1. Intracellular ROS levels in the indicated cell populations were quantified by multi parameter FACS analyses.</p

Effects of microgravity on DNA damage response in Caenorhabditis elegans during Shenzhou-8 spaceflight

<div><p></p><p><i>Purpose</i>: Space radiations and microgravity both could cause DNA damage in cells, but the effects of microgravity on DNA damage response to space radiations are still controversial.</p><p><i>Materials and methods</i>: A mRNA microarray and microRNA micro- array in dauer larvae of <i>Caenorhabditis elegans (C. elegans)</i> that endured spaceflight environment and space radiations environment during 16.5-day Shenzhou-8 space mission was performed.</p><p><i>Results</i>: Twice as many transcripts significantly altered in the spaceflight environment than space radiations alone. The majority of alterations were related to protein amino acid dephosphorylation and histidine metabolic and catabolic processes. From about 900 genes related to DNA damage response, 38 differentially expressed genes were extracted; most of them differentially expressed under spaceflight environment but not space radiations, although the identical directions of alteration were observed in both cases. cel-miR-81, cel- miR-82, cel-miR-124 and cel-miR-795 were predicted to regulate DNA damage response through four different anti-correlated genes.</p><p><i>Conclusions</i>: Evidence was provided that, in the presence of space radiations, microgravity probably enhanced the DNA damage response in <i>C. elegans</i> by integrating the transcriptome and microRNome.</p></div