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The capability of misalignment tolerance between the primary and secondary coils in an inductive power transfer system is vital. This paper proposes a novel coupling structure composed of a solenoid and a planar square coil with a third coil (SPS-TC) that can significantly improve the misalignment tolerance of couplers. The novelty of SPS-TC is the combination of concentrated magnetic fields and reverse magnetic fields. The proposed SPS-TC has an excellent characteristic that when coils are misaligned in the horizontal direction, the coupling coefficient varies within a very small range. A 1-kW prototype is fabricated. The experimental results show that when the horizontal misaligned distance does not exceed 37.5% of the coil size, the output voltage variation range is extremely small, and the minimum system efficiency is 90.12%. The benefits of SPS-TC are a smaller outer side length and excellent horizontal and rotational misalignment tolerance. It can be used for wireless charging applications in robots, rockets, satellites, unmanned aerial vehicles, etc.

•Double-sided spray cooling system for airborne electronics is built.•Cooling effects under sub-atmospheric and atmospheric pressures are tested.•Spray cooling under sub-atmospheric pressure is better.

Progesterone receptor membrane component 1 (PGRMC1) interacts with PGRMC2, and disrupting this interaction in spontaneously immortalized granulosa cells (SIGCS) leads to an inappropriate entry into the cell cycle, mitotic arrest, and ultimately cell death. The present study revealed that PGRMC1 and PGRMC2 localize to the cytoplasm of murine granulosa cells of nonatretric follicles with their staining intensity being somewhat diminished in granulosa cells of atretic follicles. Compared to controls (Pgrmc1fl/fl), the rate at which granulosa cells entered the cell cycle increased in nonatretic and atretic follicles of mice in which Pgrmc1 was conditionally deleted (Pgrmc1d/d) from granulosa cells. This increased rate of entry into the cell cycle was associated with a ≥ 2-fold increase in follicular atresia and the nuclear localization of nuclear factor-kappa-B transcription factor P65; (NFΚB/p65, or RELA). GTPase activating protein binding protein 2 (G3BP2) binds NFΚB/p65 through an interaction with NFΚB inhibitor alpha (IκBα), thereby maintaining NFΚB/p65's cytoplasmic localization and restricting its transcriptional activity. Since PGRMC1 and PGRMC2 bind G3BP2, studies were designed to assess the functional relationship between PGRMC1, PGRMC2, and NFΚB/p65 in SIGCs. In these studies, disrupting the interaction between PGRMC1 and PGRMC2 increased the nuclear localization of NFΚB/p65, and depleting PGRMC1, PGRMC2, or G3BP2 increased NFΚB transcriptional activity and the progression into the cell cycle. Taken together, these studies suggest that PGRMC1 and 2 regulate granulosa cell cycle entry in follicles by precisely controlling the localization and thereby the transcriptional activity of NFΚB/p65.

Despite recent vigorous progress in synthesis of monofunctional electrocatalysts for hydrogen evolution reaction (HER) or oxygen evolution reaction (OER), it remains challenging to develop bifunctional electrocatalysts for efficient overall water splitting. Herein, we report the crafting of MoC2-doped NiFe alloy nanoparticles (NPs) encapsulated within a-few-layer-thick N-doped graphene (denoted NG-NiFe@MoC2) via one-step calcination of hybrid precursors containing polymer-encapsulating binary Prussian blue analogues NPs and Mo6+cations. The resulting NG-NiFe@MoC2nanohybrids were exploited as electrocatalysts and exhibited excellent performance on either HER or OER separately as a direct consequence of the synergistic effects of unique compositions (i.e., MoC2dopants and NiFe alloy NPs; both exerted profound influence on HER and OER) and advantageous architecture (i.e., a-few-layer-thick N-doped graphene encapsulating shell). Remarkably, an alkaline electrolyte capitalizing on NG-NiFe@MoC2nanohybrids as bifunctional electrocatalysts achieved overall water-splitting (i.e., concurrent HER and OER) current density of 10 mA cm−2at a low potential of 1.53 V over a period of 10-h operation, outperforming the precious Pt/C//RuO2counterpart.

The present studies were designed to determine whether progesterone (P4)-progesterone receptor membrane component 1 (PGRMC1) signaling is able to attenuate the apoptotic effects of oxidative stress induced by hydrogen peroxide (H2O2). To achieve this goal, freshly isolated human granulosa/luteal cells were maintained in culture. After several passages, the cells were treated with H2O2, which induced apoptosis within 2.5 h, while simultaneous treatment with P4 attenuated the apoptotic action of H2O2. AG 205, a PGRMC1 antagonist, eliminated P4's ability to prevent H2O2-induced apoptosis. AG 205 neither affected PGRMC1's cytoplasmic localization nor its interaction with PGRMC2, but appeared to reduce its presence within the nucleus. AG 205 also (1) increased the monomeric and decreased the higher molecular weight forms of PGRMC1 (i.e., dimers/oligomers) and (2) altered the expression of several genes involved in apoptosis. The most dramatic change was an approximate 8-fold increase in Harakiri (Hrk) mRNA. However, AG 205 did not induce apoptosis in the absence of H2O2. Taken together, these observations suggest that the higher molecular weight forms of PGRMC1 likely account in part for PGRMC1's ability to suppress the expression of Hrk. Harakiri is a BH-3 only member of the B-cell lymphoma 2 (BCL2) family that promotes apoptosis by binding to and antagonizing the antiapoptotic action of BCL2- and BCL2-like proteins. It is likely then that PGRMC1's ability to suppress Hrkis part of the mechanism through which P4-PGRMC1 signaling preserves the viability of human granulosa/luteal cells.The PGRMC1 antagonist, AG 205, blocks the ability of P4 to inhibit H2O2-induced apoptosis by disrupting PGRMC1 dimers/oligomers and inducing the expression of the apoptosis inducing BH3-only protein, Harakiri.

The adenine nucleotide translocator (ANT), which has not been well studied in hymenopteran insects, catalyzes the transport of ATP and ADP across the impermeable mitochondrial membrane and plays a key role in the regulation of reactive oxygen species (ROS) generation and cell death. In this study, we isolated and characterized a single-copy ANTgene, referred as AccANT, from Apis cerana cerana(Fabricius) (Hymenoptera: Apidae). An alignment analysis showed that the deduced AccANT amino acid sequence has high identity with other known ANTs. Based on the genomic DNA sequence, a partial 5′-flanking region was obtained and some putative cis-acting elements related to the development and stresses were also predicted. Real-time quantitative PCR analysis indicated that the accumulation of AccANTtranscripts could be detected in all development stages but reached its highest level in 1-day-old adult worker honey bees. Simultaneously, AccANTwas also primarily localized in the thorax tissue of adults. Moreover, AccANTexpression was found to be induced in response to temperature stress and H2O2injection. These results suggest that AccANTmay be involved in the regulation of development and in reducing ROS generation when suffering from environmental stress.

Previous studies have shown that extracts of the aromatic herb feverfew (Tanacetum parthenium) and one of its bioactive components, parthenolide, have anti-inflammatory properties in vivo and in vitro. We examined both crude feverfew extracts and purified parthenolide for their ability to modulate adhesion molecule expression in human synovial fibroblasts. Pretreatment of synovial fibroblasts with either feverfew extracts or purified parthenolide could inhibit the expression of intercellular adhesion molecule-1 (ICAM-1) induced by the cytokines IL-1 (up to 95% suppression), TNF-α (up to 93% suppression), and, less strongly, interferon-γ (up to 39% suppression). Inhibition of ICAM-1 was dose and time dependent; as little as a 30-min pretreatment with feverfew resulted in inhibition of ICAM-1. The decrease in ICAM-1 expression was accompanied by a decrease in T-cell adhesion to the treated fibroblasts. Other herbal extracts with reported anti-inflammatory effects were similarly tested and did not decrease ICAM-1 expression. The modulation of adhesion molecule expression may be an additional mechanism by which feverfew mediates anti-inflammatory effects.

A series of crown ether cyanine dyes including crown ether styryl cyanine dyes, crown ether merocyanine dyes and crown ether squarylium cyanine dyes unsymmetric and symmetric derived from key intermediate 2methyl5,615crown5benzotellurazole 1 were prepared.

This study was conducted under field conditions to determine the effect of 20 derivatives of selenamorpholine on selenium (Se) concentration in radish as compared to sodium selenite sources of Se. Most of the organoselena compounds were more effective for the uptake of selenium by radish than sodium selenite. Sprayed with 100 mL 50 ppm 4-(l-bromoundecanoyl) selenamorpholine, the Se content of the leaf of radish increased from 0.17 ppm to 124.04 ppm. Sprayed with 4-benzoyl selenamorpholine and selenamorpholine hydrochloride, the Se content of the stem tuber increased from 4.34 ppm to 30.96 ppm and 28.75 ppm, respectively.

Abstract: Objective: To observe the effect of Yiqi Huoxue (replenishing Qi and activating blood circulation, YQHX) recipe in patients with advanced stage of esophageal cancer treated with radiotherapy and intervention chemotherapy.Methods: In comparing 31 patients who were treated with radio-chemotherapy (RCT, Group A), and 31 patients treated with RCT plus YQHX recipe (Group B).Results: Immediate effective rates were 48.4 % in Group A and 64.5 % in Group B(P>0.05). The function of bone marrow in Group B was obviously better than that in Group A. The 1 year metastasis rate in Group A was higher than that in Group B, but the long-term survival rate of Group B was obviously higher than that in Group A (P<0.05).Conclusion: YQHX recipe could reduce the bone marrow suppression caused by RCT, lower the metastasis rate, prolong the long-term survival and improve the quality of life.

Dekking and Meester defined six phases for a subclass of random Cantor sets consisting of those generated by Bernoulli random substitutions. They proved that the random Sierpinski carpet passed through all these phases asp tended from 0 to 1, but the were not able to prove the existencne of phase V in the Mandelbrot percolation process. In this paper, we accomplish the proof by improving their methods.

This paper contains a proof of the conjecture concerning the non-coexistence of one dimensional multicolor contact processes. The main technique of the proof is that the “2's” dcuble active path dominates the oriented percolation.

The ability to create nanomaterials with hollow micro- or nanostructures renders their applications in fields such as catalysis, controlled delivery and lightweight composites. Herein, we report a simple three-step route to Cu2O/Cu nanotubes populated by interconnected, phosphorus-doped CoO nanoparticles (denoted P–CoO–Cu2O/Cu-NTs). They possess three-dimensional (3D) accessible surface, thereby greatly favoring the exposure of active sites and electrolyte transport for efficient electrocatalysis. Notably, the integrated electrochemical tests and theoretical calculation reveal that the P-doping imparts the optimization of the electronic structures of CoO, enhancing its conductivity, facilitating the in-situ formation of active CoOOH species during oxygen evolution reaction (OER), and suitably regulating free energy for adsorption of the OER intermediates. Consequently, the P–CoO–Cu2O/Cu-NTs exhibit outstanding performance for OER and urea oxidation reaction (UOR) with the overpotential of 261 mV and potential of 1.43 V vs RHE, respectively, at 10 mA cm−2, outperforming most of non-precious metal electrocatalysts and RuO2. As such, the three-step approach involving the use of Cu nanowires as template to yield Cu2O/Cu nanotubular yet porous scaffold may stand out as a robust strategy for judicious crafting of interconnected heteroatom-doped metal oxides for high-performance electrocatalysis.

The present studies were designed to determine the role of progesterone receptor membrane component 1 (PGRMC1), PGRMC2, progestin and adipoQ receptor 7 (PAQR7), and progesterone receptor (PGR) in mediating the antimitotic action of progesterone (P4) in human granulosa/luteal cells. For these studies granulosa/luteal cells of 10 women undergoing controlled ovarian hyperstimulation were isolated, maintained in culture, and depleted of PGRMC1, PGRMC2, PAQR7, or PGRby siRNA treatment. The rate of entry into the cell cycle was assessed using the FUCCI cell cycle sensor to determine the percentage of cells in the G1/S stage of the cell cycle. PGRMC1, PGRMC2, PAQR7, and PGRmRNA levels were assessed by real-time PCR and their interactions monitored by in situ proximity ligation assays (PLAs). These studies revealed that PGRMC1, PGRMC2, PAQR7, and PGRwere expressed by granulosa/luteal cells from all patients, with PGRMC1mRNA being most abundant, followed by PAQR7, PGRMC2, and PGR. However, their mRNA levels showed considerable patient variation. P4's ability to suppress entry into the cell cycle was dependent on PGRMC1, PGRMC2, and PAQR7 but not PGR. Moreover, PLAs indicated that PGRMC1, PGRMC2, and PAQR7 formed a complex within the cytoplasm. Based on these studies, it is proposed that these three P4 mediators form a complex within the cytoplasm that is required for P4's action. Moreover, P4's ability to regulate human follicle development may be dependent in part on the expression levels of each of these P4 mediators.

Progesterone receptor membrane component 1 (PGRMC1) and PGRMC2 are expressed in rat granulosa cells and spontaneously immortalized granulosa cells (SIGCs) but their biological roles are not well defined. The present studies demonstrate that depleting either Pgrmc1or Pgrmc2in SIGCs increases entry into the cell cycle but does not increase cell proliferation. Rather, PGRMC1 and/or PGRMC2-deplete cells accumulate in metaphase and undergo apoptosis. Because both PGRMC1 and PGRMC2 localize to the mitotic spindle, their absence likely accounts for cells arresting in metaphase. Moreover, pull-down assays, colocalization studies and in situ proximity ligation assays (PLA) indicate that PGRMC1 binds PGRMC2. Disrupting the PGRMC1:PGRMC2 complex through the use of siRNA or the cytoplasmic delivery of a PGRMC2 antibody increases entry into the cell cycle. Conversely, overexpressing either PGRMC1-GFP or GFP-PGRMC2 fusion protein inhibits entry into the cell cycle. Subsequent studies reveal that depleting PGRMC1 and/or PGRMC2 reduces the percentage of cells in G0and increases the percentage of cells in G1. These observations indicate that in addition to their role at metaphase, PGRMC1 and PGRMC2 are involved in regulating entry into the G1stage of the cell cycle. Interestingly, both PGRMC1 and PGRMC2 bind GTPase-activating protein-binding protein 2 (G3BP2) as demonstrated by pull-down assays, colocalization assays, and PLAs. G3bp2siRNA treatment also promotes entry into the G1stage. This implies that dynamic changes in the interaction among PGRMC1, PGRMC2, and G3BP2 play an important protein regulating the rate at which SIGCs enter into the cell cycle.

Progesterone receptor membrane component 2 (Pgrmc2) mRNA was detected in the immature rat ovary. By 48 h after eCG, Pgrmc2mRNA levels decreased by 40% and were maintained at 48 h post-hCG. Immunohistochemical studies detected PGRMC2 in oocytes and ovarian surface epithelial, interstitial, thecal, granulosa, and luteal cells. PGRMC2 was also present in spontaneously immortalized granulosa cells, localizing to the cytoplasm of interphase cells and apparently to the mitotic spindle of cells in metaphase. Interestingly, PGRMC2 levels appeared to decrease during the G1stage of the cell cycle. Moreover, overexpression of PGRMC2 suppressed entry into the cell cycle, possibly by binding the p58 form of cyclin dependent kinase 11b. Conversely, Pgrmc2small interfering RNA (siRNA) treatment increased the percentage of cells in G1and M stage but did not increase the number of cells, which was likely due to an increase in apoptosis. Depleting PGRMC2 did not inhibit cellular 3H-progesterone binding, but attenuated the ability of progesterone to suppress mitosis and apoptosis. Taken together these studies suggest that PGRMC2 affects granulosa cell mitosis by acting at two specific stages of the cell cycle. First, PGRMC2 regulates the progression from the G0into the G1stage of the cell cycle. Second, PGRMC2 appears to localize to the mitotic spindle, where it likely promotes the final stages of mitosis. Finally, siRNA knockdown studies indicate that PGRMC2 is required for progesterone to slow the rate of granulosa cell mitosis and apoptosis. These findings support a role for PGRMC2 in ovarian follicle development.

Progesterone receptor membrane component 1 (PGRMC1) mediates the antiapoptotic action of progesterone (P4). PGRMC1 interacts with plasminogen activator inhibitor 1 RNA-binding protein (PAIRBP1), but the functional significance of this interaction is unknown. To examine the function of PGRMC1-PAIRBP1 interaction, PAIRBP1 was depleted from spontaneously immortalized granulosa cells (SIGCs) and the effects on the expression and localization of PGRMC1 as well as P4's ability to bind to SIGCs and prevent apoptosis was assessed. Depleting PAIRBP1 enhanced cellular 3H-P4 binding and did not alter the expression or cellular localization of PGRMC1 but attenuated P4's antiapoptotic action. Transfection of a PGRMC1-green fluorescent protein (GFP) peptide mimic, which binds PAIRBP1 as demonstrated by in situ proximity assay, doubled the rate at which SIGCs undergo apoptosis compared to cells transfected with either the empty GFP expression vector or Pairbp1small interfering RNA. Moreover, P4 did not prevent these cells from undergoing apoptosis. Similar studies conducted with granulosa cells isolated from immature rats also showed that PGRMC1 interacts with PAIRBP1 and that transfection of PGRMC1-GFP peptide mimic accelerates the rate of granulosa cell apoptosis by 4-fold even in the presence of serum and P4. These studies support the concept that the interaction between PAIRBP1-PGRMC1 is an essential component of the mechanism through which P4 inhibits apoptosis. Surprisingly, PGRMC1-PAIRBP1 interaction is not required for P4 binding or the cellular localization of PGRMC1 but rather appears to couple PGRMC1 to downstream components of the P4-PGRMC1 signal transduction pathway.

ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.

ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.