Reentrance of interface superconductivity in a high-Tc cuprate heterostructure.

Increasing the carrier density in a Mott insulator by chemical doping gives rise to a generic superconducting dome in high temperature superconductors. An intriguing question is whether a second superconducting dome may exist at higher dopings. Here we heavily overdope La2-xSrxCuO4 (0.45 ≤ x ≤ 1.0) and discover an unprecedented reentrance of interface superconductivity in La2-xSrxCuO4 /La2CuO4 heterostructures. As x increases, the superconductivity is weakened and completely fades away at x = 0.8; but it revives at higher doping and fully recovers at x = 1.0. This is shown to be correlated with the suppression of the interfacial charge transfer around x = 0.8 and the weak-to-strong localization crossover in the La2-xSrxCuO4 layer. We further construct a theoretical model to account for the sophisticated relation between charge localization and interfacial charge transfer. Our work advances both the search for and control of new superconducting heterostructures.

[Establishment and validation of a preoperative nomogram model for predicting the risk of hepatocellular carcinoma with microvascular invasion].

Objective: To establish and validate a nomogram model for predicting the risk of microvascular invasion(MVI) in hepatocellular carcinoma. Methods: The clinical data of 210 patients with hepatocellular carcinoma who underwent hepatectomy at Department of Hepatobiliary and Pancreatic Surgery,the Affiliated Hospital of Qingdao University from January 2013 to October 2021 were retrospectively analyzed. There were 169 males and 41 females, aged(M(IQR)) 57(12)years(range:30 to 80 years). The patients were divided into model group(the first 170 cases) and validation group(the last 40 cases) according to visit time. Based on the clinical data of the model group,rank-sum test and multivariate Logistic regression analysis were used to screen out the independent related factors of MVI. R software was used to establish a nomogram model to predict the preoperative MVI risk of hepatocellular carcinoma,and the validation group data were used for external validation. Results: Based on the modeling group data,the receiver operating characteristic curve was used to determine that cut-off value of DeRitis ratio,γ-glutamyltransferase(GGT) concentration,the inverse number of activated peripheral blood T cell ratio (-aPBTLR) and the maximum tumor diameter for predicting MVI, which was 0.95((area under curve, AUC)=0.634, 95%CI: 0.549 to 0.719), 38.2 U/L(AUC=0.604, 95%CI: 0.518 to 0.689),-6.05%(AUC=0.660, 95%CI: 0.578 to 0.742),4 cm(AUC=0.618, 95%CI: 0.533 to 0.703), respectively. Univariate and multivariate Logistic regression analysis showed that DeRitis≥0.95,GGT concentration ≥38.2 U/L,-aPBTLR>-6.05% and the maximum tumor diameter ≥4 cm were independent related factors for MVI in hepatocellular carcinoma patients(all P<0.05). The nomogram prediction model based on the above four factors established by R software has good prediction efficiency. The C-index was 0.758 and 0.751 in the model group and the validation group,respectively. Decision curve analysis and clinical impact curve showed that the nomogram model had good clinical benefits. Conclusions: DeRitis ratio,serum GGT concentration,-aPBTLR and the maximum tumor diameter are valuable factors for preoperative prediction of hepatocellular carcinoma with MVI. A relatively reliable nomogram prediction model could be established on them.

Manipulating topological transformations of polar structures through real-time observation of the dynamic polarization evolution.

Topological structures based on controllable ferroelectric or ferromagnetic domain configurations offer the opportunity to develop microelectronic devices such as high-density memories. Despite the increasing experimental and theoretical insights into various domain structures (such as polar spirals, polar wave, polar vortex) over the past decade, manipulating the topological transformations of polar structures and comprehensively understanding its underlying mechanism remains lacking. By conducting an in-situ non-contact bias technique, here we systematically investigate the real-time topological transformations of polar structures in PbTiO3/SrTiO3 multilayers at an atomic level. The procedure of vortex pair splitting and the transformation from polar vortex to polar wave and out-of-plane polarization are observed step by step. Furthermore, the redistribution of charge in various topological structures has been demonstrated under an external bias. This provides new insights for the symbiosis of polar and charge and offers an opportunity for a new generation of microelectronic devices.

Intensified nitrate and phosphorus removal in an electrolysis -integrated horizontal subsurface-flow constructed wetland.

A novel electrolysis-integrated horizontal subsurface-flow constructed wetland system (E-HFCWs) was developed for intensified removal of nitrogen and phosphorus contaminated water. The dynamics of nitrogen and phosphorus removal and that of main water qualities of inflow and outflow were also evaluated. The hydraulic retention time (HRT) greatly enhanced nitrate removal when the electrolysis current intensity was stabilized at 0.07 mA/cm2. When the HRT ranged from 2 h to 12 h, the removal rate of nitrate increased from 20% to 84%. Phosphorus (P) removal was also greatly enhanced-exceeding 90% when the HRT was longer than 4 h in the electrolysis-integrated HFCWs. This improved P removal is due to the in-situ formation of ferric ions by anodizing of sacrificial iron anodes, causing chemical precipitation, physical adsorption and flocculation of phosphorus. Thus, electrolysis plays an important role in nitrate and phosphorus removal. The diversity and communities of bacteria in the biofilm of substrate was established by the analysis of 16S rDNA gene sequences, and the biofilm was abundant with Comamonadaceae and Xanthomonadaceae bacteria in E-HFCWs. Test results illustrated that the electrolysis integrated with horizontal subsurface-flow constructed wetland is a feasible and effective technology for intensified nitrogen and phosphorus removal.

High performance of nitrogen and phosphorus removal in an electrolysis-integrated biofilter.

A novel electrolysis-integrated biofilter system was developed in this study to evaluate the intensified removal of nitrogen and phosphorus from contaminated water. Two laboratory-scale biofilter systems were established, one with electrolysis (E-BF) and one without electrolysis (BF) as control. The dynamics of intensified nitrogen and phosphorus removal and the changes of inflow and outflow water qualities were also evaluated. The total nitrogen (TN) removal rate was 94.4% in our newly developed E-BF, but only 74.7% in the control BF. Ammonium removal rate was up to 95% in biofilters with or without electrolysis integration with an influent ammonium concentration of 40 mg/L, and the accumulation of nitrate and nitrite was much lower in the effluent of E-BF than that of BF. Thus electrolysis plays an important role in TN removal especially the nitrate and nitrite removal. Phosphorus removal was significantly enhanced, exceeding 90% in E-BF by chemical precipitation, physical adsorption, and flocculation of phosphorus because of the in situ formation of ferric ions by the anodizing of sacrificial iron anodes. Results from this study indicate that the electrolysis integrated biofilter is a promising solution for intensified nitrogen and phosphorus removal.

Agriculture facilitated permanent human occupation of the Tibetan Plateau after 3600 B.P.

Our understanding of when and how humans adapted to living on the Tibetan Plateau at altitudes above 2000 to 3000 meters has been constrained by a paucity of archaeological data. Here we report data sets from the northeastern Tibetan Plateau indicating that the first villages were established only by 5200 calendar years before the present (cal yr B.P.). Using these data, we tested the hypothesis that a novel agropastoral economy facilitated year-round living at higher altitudes since 3600 cal yr B.P. This successful subsistence strategy facilitated the adaptation of farmers-herders to the challenges of global temperature decline during the late Holocene.

Visible-light-enhanced gating effect at the LaAlO3/SrTiO3 interface.

Electrostatic gating field and light illumination are two widely used stimuli for semiconductor devices. Via capacitive effect, a gate field modifies the carrier density of the devices, while illumination generates extra carriers by exciting trapped electrons. Here we report an unusual illumination-enhanced gating effect in a two-dimensional electron gas at the LaAlO3/SrTiO3 interface, which has been the focus of emergent phenomena exploration. We find that light illumination decreases, rather than increases, the carrier density of the gas when the interface is negatively gated through the SrTiO3 layer, and the density drop can be 20 times as large as that caused by the conventional capacitive effect. This effect is further found to stem from an illumination-accelerated interface polarization, an originally extremely slow process. This unusual effect provides a promising controlling of the correlated oxide electronics in which a much larger gating capacity is demanding due to their intrinsic larger carrier density.

Ischemic preconditioning reduces deep hypothermic circulatory arrest cardiopulmonary bypass induced lung injury.

PURPOSE: Ischemic preconditioning (IP) has been used to reduce ischemia-reperfusion injury in several models. It remains unknown whether IP is sufficient to prevent deep hypothermic circulatory arrest (DHCA) cardiopulmonary bypass (CPB) induced lung injury. MATERIALS AND METHODS: Twenty-four piglets were randomly divided into four groups: routine CPB (CPB), CPB + DHCA (DHCA), CPB + IP + DHCA (IP-1) and CPB + hypoxia-ischemia preconditioning + DHCA (IP-2). Lung static compliance (Cstat) and pulmonary vascular resistance (PVR) were measured as indicators of lung function at three points during CPB. TNF-α, IL-8 and IL-10 expressions were detected by radioimmunoassay. CD18 expression was determined by flow cytometer. Some lung tissues were excised to measure the wet/dry weight ratio (W/D) and some were fixed to observe pathological changes. RESULTS: Cstat significantly decreased whereas PVR increased in DHCA group. IP prevented DHCA-induced lung functional impairment, especially IP-2 treatment. More cytokines were produced after CPB in all groups, but with varying level. Left atrium/pulmonary artery ratio of CD18 expression on monocytes decreased only in DHCA group, whereas which on polymorphonuclear neutrophils decreased in DHCA group, IP-1 group at 1h post-CPB and IP-2 group. Although lung W/D was increased in IP-2 group compared with pre-CPB, but significantly lower than that in DHCA group. Histological findings showed less lung injuries in IP groups than DHCA group. CONCLUSIONS: DHCA aggravates lung inflammatory injury and IP may reverse this injury. Maintaining ventilation with pulmonary artery perfusion in the lung IP process during CPB seems to be more superior to single pulmonary artery perfusion.

Titanium dxy ferromagnetism at the LaAlO3/SrTiO3 interface.

A number of recent transport and magnetization studies have shown signs of ferromagnetism in the LaAlO3/SrTiO3 heterostructure, an unexpected property with no bulk analogue in the constituent materials. However, no experiment thus far has provided direct information on the host of the magnetism. Here we report spectroscopic investigations of the magnetism using element-specific techniques, including X-ray magnetic circular dichroism and X-ray absorption spectroscopy, along with corresponding model calculations. We find direct evidence for in-plane ferromagnetic order at the interface, with Ti(3+) character in the dxy orbital of the anisotropic t2g band. These findings establish a striking example of emergent phenomena at oxide interfaces.

Vasorelaxing effects of Caesalpinia sappan involvement of endogenous nitric oxide.

Methanolic extract and two purified compounds (brazilin and hematoxylin) from Caesalpinia sappan were examined for their relaxant effects in isolated rat thoracic aorta. The methanolic extract significantly and dose-dependently relaxed the alpha1-receptor agonist phenylephrine-precontracted aortic rings, without affecting passive tension of these vessels. Removal of the vascular endothelium, inhibition of nitric oxide (NO) synthase with 0.1 mM Nomega-nitro-L-arginine and of cGMP biosynthesis with 10 microM methylene blue abolished the vasorelaxant effects of the herbal extract at doses up to 30 microg/ml. Similar vasorelaxant effects were observed with brazilin and hematoxylin. Therefore, these results suggest that brazilin and hematoxylin may be responsible for the vascular relaxant effects of C. sappan, via endogenous NO and subsequent cGMP formation. The vascular relaxant effects of the plant may contribute to its therapeutic actions.

Nitric oxide as a regulator of tissue oxygen consumption.

Nitric oxide originating from the microvascular endothelium and other tissue sources appears to play an important physiological role in the regulation of mitochondrial respiration in vivo. Physiological processes and pathophysiological conditions that influence the production and action of nitric oxide are likely to alter the control of tissue respiration by nitric oxide. Oxidant stress associated with the production of peroxynitrite from nitric oxide, under conditions such as hypoxia-reoxygenation, convert the reversible inhibition of respiration by nitric oxide into an irreversible process, which is potentially an important contributor to the expression of alterations in physiological function and tissue injury.

Inhibition of rat cardiac muscle contraction and mitochondrial respiration by endogenous peroxynitrite formation during posthypoxic reoxygenation.

This study was designed to investigate the potential role of endogenous peroxynitrite (ONOO-) formation in the inhibition of cardiac muscle contractility and mitochondrial respiration during posthypoxic reoxygenation. Isometric contraction of isolated rat left ventricular posterior papillary muscle was virtually eliminated at the end of an exposure to 15 minutes of hypoxia and remained 40+/-5% depressed an hour after the reintroduction of O2. O2 uptake by rat left ventricular cardiac muscle, measured by a Clark-type O2 electrode, was also inhibited by 24+/-2% at 10 minutes after reoxygenation. The inhibition of contractility and respiration during posthypoxic reoxygenation was markedly attenuated by the NO synthase inhibitor nitro-L-arginine, exogenous superoxide dismutase, and the ONOO- scavenger urate but not by the hydroxyl radical scavenger mannitol. Generation of ONOO- with the NO donor S-nitroso-N-acetylpenicillamine (SNAP) plus the superoxide-releasing agent pyrogallol caused an irreversible inhibition of cardiac contractile and respiratory function. Unlike ONOO-, exogenous (SNAP) and endogenous (bradykinin) sources of NO inhibited contractility in a reversible manner. Under conditions of comparable amounts of respiratory inhibition in unstimulated incubated muscle, the NO-dependent agents and the mitochondrial antagonist NaCN produced a smaller degree of suppression of contractility compared with ONOO- and posthypoxic reoxygenation. These results are consistent with a contributing role for endogenous ONOO- formation in the inhibition of cardiac muscle contractility and mitochondrial respiration during posthypoxic reoxygenation.

ACE inhibitors promote nitric oxide accumulation to modulate myocardial oxygen consumption.

BACKGROUND: ACE inhibitors potentiate kinin-nitric oxide (NO)-dependent coronary vascular dilation, and NO can modulate myocardial oxygen consumption. Whether ACE inhibitors also affect myocardial O2 consumption has not been established. METHODS AND RESULTS: Production of nitrite, a metabolite of NO in aqueous solution, in coronary microvessels and O2 consumption in myocardium were quantified with the use of in vitro tissue preparations, the Greiss reaction, and a Clark-type O2 electrode. In coronary microvessels, kininogen (the precursor of kinin; 10 micrograms/mL) and three ACE inhibitors (captopril, enalaprilat, or ramiprilat; 10(-8) mol/L) increased nitrite production from 76 +/- 6 to 173 +/- 15, 123 +/- 12, 125 +/- 12, and 153 +/- 12 pmol/mg, respectively (all P < .05). In myocardium, kininogen (10 micrograms/mL) and captopril, enalaprilat, or ramiprilat (10(-4) mol/L) reduced cardiac O2 consumption by 41 +/- 2%, 19 +/- 3%, 25 +/- 2%, and 35 +/- 2%, respectively. The changes in both nitrite release and O2 consumption in vitro were blocked by N omega-nitro-L-arginine methyl ester or N omega-nitro-L-arginine, inhibitors of endogenous NO formation. The effects were also blocked by HOE 140, which blocks the bradykinin B2-kinin receptor, and serine protease inhibitors, which inhibit local kinin formation. CONCLUSIONS: Our data indicate that stimulation of local kinin formation by use of a precursor for kinin formation or inhibition of kinin degradation by use of ACE inhibitors increases NO formation and is important in the control of cardiac O2 consumption. Vasodilation and control of myocardial O2 consumption by NO may contribute importantly to the therapeutic actions of ACE inhibitors in cardiac disease states.

Role of nitric oxide and its interaction with superoxide in the suppression of cardiac muscle mitochondrial respiration. Involvement in response to hypoxia/reoxygenation.

BACKGROUND: Nitric oxide (NO); superoxide anion (O2.d-); the reaction product of NO with O2.d-, peroxynitrite (ONOO-); and ischemia/reperfusion have all been reported to inhibit respiration in isolated mitochondria. However, the specific species involved in the inhibition of respiration in intact tissues are poorly understood. METHODS AND RESULTS: O2 consumption in isolated cardiac muscle from bovine calf hearts was quantified by use of a Clark-type electrode. Exogenous and endogenous sources of NO, from S-nitroso-N-acetylpenicillamine (SNAP) and bradykinin or carbachol, reversibly inhibited respiration, whereas the O2.- releasing agent, pyrogallol (PG), inhibited respiration in a manner that was only partially reversed when examined 15 minutes after the removal of PG. The generation of ONOO- with SNAP + PG caused a potentiation of the O2(-)-elicited inhibition of respiration when examined 15 minutes after the removal of the ONOO- generating system. Tiron (a scavenger of O2.-) did not alter the actions of SNAP, but it attenuated the direct inhibitory effects of PG +/- SNAP and essentially eliminated the suppression of respiration observed 15 minutes after removal of the O2.- or ONOO- generating system. Urate (a scavenger of ONOO-) antagonized only the actions of PG + SNAP. After exposure of muscle slices to a model of hypoxia (15 minutes) and reoxygenation (10 minutes), respiratory inhibition was observed. This reoxygenation-induced inhibition was potentiated by L-arginine, the substrate for NO biosynthesis, and was markedly blocked by nitro-L-arginine (an NO synthase inhibitor), Tiron, or urate. CONCLUSIONS: The potentially physiological reversible regulation of respiration in cardiac muscle by NO is converted to an effect that does not show rapid reversibility under conditions in which ONOO- forms, and this could contribute to cardiac dysfunction in situations such as hypoxia/reoxygenation.

Role of endothelium-derived nitric oxide in the modulation of canine myocardial mitochondrial respiration in vitro. Implications for the development of heart failure.

The mechanism responsible for the regulation of cardiac function by endogenous nitric oxide (NO) remains unclear. In this investigation, O2 consumption by freshly isolated myocardial muscle segments from the left ventricular free wall of canine hearts was quantified by a Clark-type O2 electrode at 37 degrees C. S-nitroso-N-acetylpenicillamine (SNAP, 9 +/- 3% to 50 +/- 8%), bradykinin (BK, 14 +/- 3% to 30 +/- 5%), or carbachol (CCh, 15 +/- 4% to 29 +/- 4%) significantly attenuated tissue O2 consumption at doses of 10(-7) to 10(-4) mol/L (mean +/- SE, P < .05). The effects of BK and CCh, but not SNAP, were blocked by 10(-4) mol/L NG-nitro-L-arginine, consistent with both BK and CCh stimulating NO biosynthesis and with SNAP decomposing to release NO, respectively. Similar doses of 8-Br-cGMP caused a respiratory inhibition, but to a lesser extent (9 +/- 2% to 14 +/- 6%). A mitochondrial uncoupler, 2,4-dinitrophenol (at 1 mmol/L), blocked the effects of 8-Br-cGMP, but not those of SNAP, BK, or CCh, suggesting that the major site of action of NO is on mitochondrial electron transport. Myocardial muscle from dogs with pacing-induced heart failure had a basal O2 consumption rate of 251 +/- 21 nmol.min-1.g-1, which was 54% higher than the rate seen in muscle from normal healthy canine hearts. The inhibitory effects of BK and CCh on O2 consumption were not observed in failing cardiac tissue, but SNAP showed an unaltered inhibitory effect. Therefore, our results indicate that NO released from microvascular endothelium by BK, stimulation of muscarinic receptors, and perhaps flow velocity may play an important physiological role in the control of cardiac mitochondrial respiration, and the loss of this regulatory function may contribute to the development of heart failure.