Extremum seeking control of quantum gates

To be useful for quantum computation, gate operations must be maintained at high fidelities over long periods of time. In addition to decoherence, slow drifts in control hardware leads to inaccurate gates, causing the quality of operation of as-built quantum computers to vary over time. Here, we demonstrate a data-driven approach to stabilized control, combining extremum-seeking control (ESC) with direct randomized benchmarking (DRB) to stabilize two-qubit gates under unknown control parameter fluctuations. As a case study, we consider these control strategies in the context of a trapped ion quantum computer using physically-realistic simulation. We then experimentally demonstrate this control strategy on a state-of-the-art, commercial trapped-ion quantum computer.Comment: 5 pages, 6 figure

FSHR and LHR Expression and Signaling as Well as Maturation and Apoptosis of Cumulus-Oocyte Complexes Following Treatment with FSH Receptor Binding Inhibitor in Sheep

Background/Aims: Currently, it remains unknown whether FSH receptor binding inhibitor (FRBI) influences follicular development and reproduction functions in humans and animals. The present study aimed to investigate FRBI effects on in vitro maturation (IVM) and apoptosis of cumulus-oocyte complexes (COCs) of sheep, to determine the effect of FRBI on mRNA and protein levels of FSHR and LHR in COCs, and to elucidate the signal pathway of FRBI effects. Methods: COCs were in vitro cultured for 24h in the IVM media supplemented with varying concentrations of FRBI (0, 10, 20, 30 and 40µg/mL) and FSH (10IU/mL). The harvested COCs were observed under an inverted microscope and maturation rates of COCs were determined. Real time RT-PCR and Western blotting were utilized to detect mRNA and protein levels of FSHR and LHR. The concentrations of FSH, LH and caspase-3 were determined using especial ELISA kits for sheep, respectively. Results: Maturation rates of COCs decreased gradually as FRBI concentrations increased from 0 to 40µg/mL, reaching a bottom value of 23.76% of the FRBI-4 group. The maximal apoptosis rate was detected in the FRBI-4 group. IP3 contents of FRBI-3 and FRBI-4 groups were reduced as compared to control group (CG) and FSH groups (P<0.05). Levels of FSHR protein of FRBI-3 and FRBI-4 groups as well as LHR protein of FRBI-4 group were significantly less than that of CG and FSH group. FSH contents of four FRBI treatment groups were gradually decreased along with the supplementation doses of FRBI. Caspase-3 contents of FRBI groups were reduced with a maximum reduction of the FRBI-2 group. Conclusion: Our results revealed supplement of FRBI into IVM media could dose-dependently decrease the maturation rate and increase apoptosis rate of sheep COCs. A lower dose of FRBI treatment slightly promoted IP3 production, but a higher dose of FRBI reduced IP3 production. FRBI suppressed the mRNA and protein expression levels of FSHR and LHR in sheep COCs. Our study will help to therapy effectively ovarian diseases, improve ovarian and follicular functions, and further to promote fertility of humans and animals

FSH receptor binding inhibitor restrains ovarian cancer through down-regulating expression levels of FSHR and ERβ in mice

389-397Follicle stimulating hormone receptor is used as an imaging biomarker for the detection of ovarian cancer (OC). Inhibiton of FSHR may attenuate the carcinogenesis particularly epithelial ovarian cancer. Here we investigated FSH receptor binding inhibitor (FRBI) effects on the follicular development, to explore their impact on expressions of FSH receptor (FSHR) and estrogen receptor b (ERβ) proteins in the ovaries. 150 female mice were assigned to FRBI+FSH (COM) group, FSH group, and control group (CG). Mice in COM-1, COM-2, and COM-3 groups were intramuscularly injected with 500, 750 and 1000 μg FRBI combined with 10 IU FSH for five consecutive days. The results showed that the numbers of secondary follicles (SF) in FSH group were increased. SF numbers of three COM groups were gradually declined as the FRBI doses rose. SF numbers of COM-2 and COM-3 groups were less than the FSH group on day 20 (P 0.05). Ovarian cortex thicknesses (OCT) of COM-3 group was less than that FSH group (P 0.05). Maximum longitudinal diameter (MLD) and transverse diameter (MTD) of SFs in three COM groups were dose-dependently decreased. FSHR protein levels of COM groups were significantly decreased as compared to FSH group (P 0.05). ERβ protein levels of COM-1 and COM-2 were less than the FSH group (P 0.05). Summarily, FRBI could reduce OCT and follicle numbers, suppress follicular development, decrease expression of ovarian ERβ and FSHR protein

Determine the Role of FSH Receptor Binding Inhibitor in Regulating Ovarian Follicles Development and Expression of FSHR and ERα in Mice

Mice of FRBI-1, FRBI-2, and FRBI-3 groups were intramuscularly injected with 20, 30, and 40mg/kg, respectively, for five consecutive days. Ovarian weights of three FRBI groups were reduced in comparison with FSH group. Ovarian cortex thicknesses (OCT) of the FRBI-3 group were less than that of the FSH group (P<0.05). As compared to FSH group, there were fewer numbers of secondary follicles (SFs) and mature follicles (MF) on the ovaries of FRBI-treated mice numbers of primary follicles (PFs) and SFs also decreased. In FRBI-3 mice, we found that the primordial follicles (POF) were scarcer, the follicles developed poorly, and granulosa cells became apoptosis. SF numbers of FRBI-2 and FRBI-3 groups were less than that of the FSH group on day 20 (P<0.05). Maximum longitudinal diameter (MLD) and transverse diameter (MTD) of three FRBI groups became decreased during the experiment. MLD and MTD of the FRBI-3 group were smaller than FSH group. Levels of FSHR mRNA and protein were less than that of CG and FSH group (P<0.05). ERα protein levels of FRBI group and serum concentrations of FSH and estradiol (E2) in the FRBI-treated mice were decreased when compared to CG and FSH group. In conclusion, FSH treatment could increase the numbers of SF and MF, enhance follicle development, reduce the numbers of SF and MF, and depress the follicular development of mice. Furthermore, FRBI declined the mRNA and protein levels of ERα and FSHR in the ovaries and dropped serum concentrations of FSH and E2 of mice

Comprehensive analysis of m6A methylomes in idiopathic pulmonary arterial hypertension

Idiopathic pulmonary arterial hypertension (IPAH) is a serious and fatal disease. Recently, m6A has been reported to play an important role in the lungs of IPAH patients and experimental pulmonary hypertension models. However, the meaning of m6A mRNAs in the peripheral blood of IPAH patients remains largely unexplored. We aimed to construct a transcriptome-wide map of m6A mRNAs in the peripheral blood of IPAH patients. M6A RNA Methylation Quantification Kit was utilized to measure the total m6A levels in the peripheral blood of IPAH patients. A combination of MeRIP-seq, RNA-seq and bioinformatics analysis was utilized to select m6A-modified hub genes of IPAH. MeRIP-qPCR and RT-qPCR were used to measure the m6A levels and mRNA levels of TP53, RPS27A, SMAD3 and FoxO3 in IPAH patients. Western blot was performed to assess the protein levels of m6A related regulators and m6A related genes in experimental PH animal models, hypoxia-treated and PDGF-BB induced PASMCs. We found that the total m6A levels were increased in peripheral blood of IPAH patients and verified that m6A levels of RPS27A and SMAD3 were significantly elevated and m6A levels of TP53 and FoxO3 were significantly reduced. The mRNA or protein levels of RPS27A, SMAD3, TP53 and FoxO3 were changed in human blood samples, experimental PH animal models and PDGF-BB induced PASMCs. Moreover, METTL3 and YTHDF1 were increased in the hypoxia induced pulmonary hypertension rat model, hypoxia-treated and PDGF-BB induced PASMCs. These finding suggested that m6A may play an important role in IPAH