Microscopic Encoding of Macroscopic Universality: Scaling Properties of Dirac Eigenspectra near QCD Chiral Phase Transition.

Macroscopic properties of the strong interaction near its chiral phase transition exhibit scaling behaviors, which are the same as those observed close to the magnetic transition in a three-dimensional classical spin system with O(4) symmetry. We show that the universal scaling properties of the chiral phase transition in quantum chromodynamics (QCD) at the macroscale are, in fact, encoded within the microscopic energy levels of its fundamental constituents, the quarks. We establish a connection between the cumulants of the chiral order parameter, i.e., the chiral condensate, and the correlations among the energy levels of quarks, i.e., the eigenspectra of the massless QCD Dirac operator. This relation elucidates how the fluctuations of the chiral condensate arise from the correlations within the infrared part of the energy spectra of quarks, and naturally leads to a generalization of the Banks-Casher relation for the cumulants of the chiral condensate. Then, through (2+1)-flavor lattice QCD calculations with varying light quark masses near the QCD chiral transition, we demonstrate that the correlations among the infrared part of the Dirac eigenvalue spectra exhibit same universal scaling behaviors as expected of the cumulants of the chiral condensate. We find that these universal scaling behaviors extend up to the physical values of the up and down quark masses. Our study reveals how the hidden scaling features at the microscale give rise to the macroscopic universal properties of QCD.

[Emotional and behavioral problems associated with sleep problems in preschool aged children].

Objective: To examine whether sleep problems are related to both emotional and behavioral problems in children aged 3-6 years. Methods: A large cross-sectional study was conducted in Anqing, Wuhu, Tongling and Yangzhou from March to June 2015. A total of 8 900 preschool aged children were included. Sleep problems were obtained by using adapted BISQ completed by the parents or the people who took care of children. Emotional and behavioral problems of the children were accessed by using Strengths and Difficulties Questionnaire (SDQ), and multivariate logistic regression model was used for statistical analyses. Results: The detected rates of emotional symptoms, conduct problems, hyperactivity problems, peer problems, total difficulties and prosocial behavior in preschool aged children were 9.0%, 13.9%, 18.9%, 25.5%, 13.6% and 16.2% respectively. All the detected rates were higher in boys than in girls except the higher rate of emotional symptoms. The proportions of children with high sleep quality, moderate sleep quality and poor or worse sleep quality were 3.9%, 52.9% and 43.2% respectively. After controlling the confounding factors of demographic variables, including gender, age, delivery mode, birth weight, birth height and patent's educational level, multinomial logistic regression analysis showed that the risk of emotional symptoms, conduct problems, hyperactivity problems, peer problems, total difficulties and prosocial behavior in children with longer sleep duration was lower than that in children with shorter sleep duration, the ORs were 0.86 (95%CI: 0.77-0.95), 0.85 (95%CI: 0.78-0.93), 0.85 (95%CI: 0.79-0.92), 0.87(95%CI: 0.81-0.93), 0.83 (95%CI: 0.76-0.91) and 0.82 (95%CI: 0.76-0.89) respectively. Compared with the children with good sleep quality, the risk of emotional symptoms, conduct problems, hyperactivity problems, peer problems, total difficulties and prosocial behavior were higher in children with poor or worse sleep quality, the ORs were 3.26 (95%CI: 2.40-4.42), 2.86 (95%CI: 2.16-3.78), 2.60 (95%CI: 2.00-3.38), 1.96 (95%CI: 1.52-2.54), 4.02 (95%CI: 3.06-5.27) and 2.56 (95%CI: 1.96-3.35) respectively. Conclusion: There was a negative impact of shorter sleep and poor or worse sleep on emotional and behavioral problems of preschool aged children.

Inhibitory effects of 2-methoxyestradiol on cell growth and invasion in human bladder cancer T-24 cells.

Recently, 2-methoxyestradiol (2-ME) has been considered to be a potential anticancer agent but has not been investigated in bladder cancer. This study was conducted to clarify the role of 2-ME in bladder cancer cells. The bladder cancer cell line T-24 was treated with 2 µm 2-ME for 2 d. The T-24 cell viability, colony formation, invasion and apoptosis were observed in 2-ME-treated and control cells. The expression of hypoxia-inducible factor 1 alpha (HIF-1α) was detected using reverse transcription-polymerase chain reaction (RT-PCR). Then western blotting assay was applied to assess expressions of HIF-1α and apoptosis factors caspase-3 and Bcl-x proteins. The mRNA and protein expressions of HIF-1α in 2-ME-treated T-24 cells were remarkably lower than that of the control cells (P < 0.05). Treatment of 2-ME could significantly inhibit T-24 the cell viability, colony formation, invasion, and promote apoptosis (all P < 0.05). In addition, the protein expression of Caspase-3 was higher and that of Bcl-x protein was lower after administration of 2-ME compared to control (both P < 0.05). Collectively, we characterized the efficacy of 2-ME on bladder cancer T-24 cells as being mediated by inhibition of cell viability, colony fomation, invasion and promoting cell apoptosis, which may be achieved by suppressing HIF-1α levels. This study suggests 2-ME as a potential drug for bladder cancer therapy.

Bortezomib enhances cancer cell death by blocking the autophagic flux through stimulating ERK phosphorylation.

The antitumor activity of an inhibitor of 26S proteasome bortezomib (Velcade) has been observed in various malignancies, including colon cancer, prostate cancer, breast cancer, and ovarian cancer. Bortezomib has been proposed to stimulate autophagy, but scientific observations did not always support this. Interactions between ERK activity and autophagy are complex and not completely clear. Autophagy proteins have recently been shown to regulate the functions of ERK, and ERK activation has been found to induce autophagy. On the other hand, sustained activation of ERK has also been shown to inhibit the maturation step of the autophagy process. In this study, we sought to identify the mechanism of autophagy regulation in cancer cells treated with bortezomib. Our results indicate that bortezomib blocked the autophagic flux without inhibiting the fusion of the autophagosome and lysosome. In ovarian cancer, as well as endometrial cancer and hepatocellular carcinoma cells, bortezomib inhibited protein degradation in lysosomes by suppressing cathepsins, which requires the participation of ERK phosphorylation, but not JNK or p38. Our findings that ERK phosphorylation reduced cathepsins further explain how ERK phosphorylation inhibits the autophagic flux. In conclusion, bortezomib may induce ERK phosphorylation to suppress cathepsin B and inhibit the catalytic process of autophagy in ovarian cancer and other solid tumors. The inhibition of cisplatin-induced autophagy by bortezomib can enhance chemotherapy efficacy in ovarian cancer. As we also found that bortezomib blocks the autophagic flux in other cancers, the synergistic cytotoxic effect of bortezomib by abolishing chemotherapy-related autophagy may help us develop strategies of combination therapies for multiple cancers.

Plasmonic (thermal) electromagnetically induced transparency in metallic nanoparticle-quantum dot hybrid systems.

We study the application of an infrared laser to control heat dissipation in a metallic nanoparticle when it is in the vicinity of a semiconductor quantum dot. The infrared laser is considered to be near-resonant with two of the conduction states of the quantum dot, coherently mixing them together. Via exciton-plasmon coupling, this process normalizes the internal field of the metallic nanoparticle, forming a plasmonic (thermal) electromagnetically induced transparency. When this process happens the metallic nanoparticle becomes nearly completely non-dissipative around its plasmon frequency, while it remains strongly dissipative at other frequencies. We show that, by adjusting the intensity of the infrared laser, one can control the transparency window width and optical Stark shift associated with such a process.

Fenofibrate attenuates endothelial monocyte adhesion in chronic heart failure: an in vitro study.

BACKGROUND: Inflammation is implicated in chronic heart failure (CHF). In this study, the potential inhibitory effect of peroxisome proliferator-activated receptor-alpha (PPARalpha) activator fenofibrate on monocyte adhesion in CHF patients was investigated in vitro. MATERIALS AND METHODS: Isolated peripheral blood mononuclear cells (PBMCs) were collected from 36 patients (aged 65 +/- 8 years) with symptomatic CHF and from 12 healthy control subjects. The cultured human aortic endothelial cells (HAECs) were stimulated with or without 2 ng mL(-1) tumour necrosis factor-alpha (TNF-alpha) and the inhibitory effects of fenofibrate at 25, 50, 100 and 200 microM on endothelial mononuclear cell adhesion were tested. Furthermore, the HAECs were stimulated with 70% sera obtained from CHF patients and control individuals, respectively, with or without pretreatments with fenofibrate. The endothelial expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) was then confirmed by mRNA expression and Western blot. RESULTS: We found that the increased adhesion of PBMCs to TNF-alpha-stimulated HAECs in CHF patients was reduced when the HAECs were pretreated with fenofibrate (31% inhibition, P = 0.0121). However, pretreatment of the isolated PBMCs collected from CHF patients with fenofibrate failed to suppress their adherence to TNF-alpha-stimulated HAECs. Furthermore, stimulation of cultured HAECs with CHF patient sera significantly increased VCAM-1 and ICAM-1 expression, which could also be inhibited by fenofibrate. CONCLUSIONS: The fenofibrate directly inhibits monocyte binding by TNF-alpha-activated HAECs, probably through preventing up-regulation of cell adhesion molecules by endothelial cells in response to inflammatory stimuli. This PPARalpha activator may have the potential to ameliorate vascular inflammation in patients with CHF.

Praseodymium hydroxide and oxide nanorods and Au/Pr6O11 nanorod catalysts for CO oxidation.

Praseodymium hydroxide nanorods were synthesized by a two-step approach: First, metallic praseodymium was used to form praseodymium chloride, which reacted subsequently with KOH solution to produce praseodymium hydroxide. In the second step the hydroxide was treated with a concentrated alkaline solution at 180 degrees C for 45 h, yielding nanorods as shown by the scanning and transmission electron microscopy images. The results of X-ray diffraction and energy-dispersive X-ray spectroscopy experiments indicate that these nanorods are pure praseodymium hydroxide with a hexagonal structure, which can be converted into praseodymium oxide (Pr6O11) nanorods of a face-centered cubic structure after calcination at 600 degrees C for 2 h in air. Gold was loaded on the praseodymium oxide nanorods using HAuCl4 as the gold source, and NaBH4 was used to reduce the gold species to metallic nanoparticles with sizes of 8-12 nm on the nanorod surface. These Au/Pr6O11 nanorods exhibit superior catalytic activity for CO oxidation.

CeO2 nanorods and gold nanocrystals supported on CeO2 nanorods as catalyst.

The formation mechanism of uniform CeO2 structure at the nanometer scale via a wet-chemical reaction is of great interest in fundamental study as well as a variety of applications. In this work, large-scale well-crystallized CeO2 nanorods with uniform diameters in the range of 20-30 nm and lengths up to tens of micrometers are first synthesized through a hydrothermal synthetic route in 5 M KOH solution at 180 degrees C for 45 h without any templates and surfactants. The nanorod formation involves dehydration of CeO2 nanoparticles and orientation growth along the 110 direction in KOH solution. Subsequently, gold nanoparticles with crystallite sizes between 10 and 20 nm are loaded on the surface of CeO2 nanorods using HAuCl4 solution as the gold source and NaBH4 solution as a reducing agent. The synthesized Au/CeO2 nanorods demonstrate a higher catalytic activity in CO oxidation than the pure CeO2 nanorods.

Apg2 is a novel protein required for the cytoplasm to vacuole targeting, autophagy, and pexophagy pathways.

To survive starvation conditions, eukaryotes have developed an evolutionarily conserved process, termed autophagy, by which the vacuole/lysosome mediates the turnover and recycling of non-essential intracellular material for re-use in critical biosynthetic reactions. Morphological and biochemical studies in Saccharomyces cerevisiae have elucidated the basic steps and mechanisms of the autophagy pathway. Although it is a degradative process, autophagy shows substantial overlap with the biosynthetic cytoplasm to vacuole targeting (Cvt) pathway that delivers resident hydrolases to the vacuole. Recent molecular genetics analyses of mutants defective in autophagy and the Cvt pathway, apg, aut, and cvt, have begun to identify the protein machinery and provide a molecular resolution of the sequestration and import mechanism that are characteristic of these pathways. In this study, we have identified a novel protein, termed Apg2, required for both the Cvt and autophagy pathways as well as the specific degradation of peroxisomes. Apg2 is required for the formation and/or completion of cytosolic sequestering vesicles that are needed for vacuolar import through both the Cvt pathway and autophagy. Biochemical studies revealed that Apg2 is a peripheral membrane protein. Apg2 localizes to the previously identified perivacuolar compartment that contains Apg9, the only characterized integral membrane protein that is required for autophagosome/Cvt vesicle formation.

Membrane recruitment of Aut7p in the autophagy and cytoplasm to vacuole targeting pathways requires Aut1p, Aut2p, and the autophagy conjugation complex.

Autophagy is a degradative pathway by which cells sequester nonessential, bulk cytosol into double-membrane vesicles (autophagosomes) and deliver them to the vacuole for recycling. Using this strategy, eukaryotic cells survive periods of nutritional starvation. Under nutrient-rich conditions, autophagy machinery is required for the delivery of a resident vacuolar hydrolase, aminopeptidase I, by the cytoplasm to vacuole targeting (Cvt) pathway. In both pathways, the vesicle formation process requires the function of the starvation-induced Aut7 protein, which is recruited from the cytosol to the forming Cvt vesicles and autophagosomes. The membrane binding of Aut7p represents an early step in vesicle formation. In this study, we identify several requirements for Aut7p membrane association. After synthesis in the cytosol, Aut7p is proteolytically cleaved in an Aut2p-dependent manner. While this novel processing event is essential for Aut7p membrane binding, Aut7p must undergo additional physical interactions with Aut1p and the autophagy (Apg) conjugation complex before recruitment to the membrane. Lack of these interactions results in a cytosolic distribution of Aut7p rather than localization to forming Cvt vesicles and autophagosomes. This study assigns a functional role for the Apg conjugation system as a mediator of Aut7p membrane recruitment. Further, we demonstrate that Aut1p, which physically interacts with components of the Apg conjugation complex and Aut7p, constitutes an additional factor required for Aut7p membrane recruitment. These findings define a series of steps that results in the modification of Aut7p and its subsequent binding to the sequestering transport vesicles of the autophagy and cytoplasm to vacuole targeting pathways.

Changes in superoxide dismutase activity and mRNA in vivo after short-term supplementation with trilinolein in rats.

BACKGROUND: Oxidative damage plays a central role in atherogenesis and antioxidation defense mechanisms may prevent atherosclerosis. This study evaluated the effect of short-term supplementation of the natural lipophilic antioxidant trilinolein on superoxide dismutase (SOD) activity and SOD-mRNA gene expression in vivo in rat vital organs. METHODS: Male Wistar rats (n = 8) were injected intraperitoneally with trilinolein (1 mM/ml/kg/day in 0.5% ethanol) daily for three consecutive days. Two control groups (n = 8) were administered saline or 0.5% ethanol in saline, respectively, for three days. RESULTS: Assay of SOD activity and SOD-mRNA by Northern blotting in rat liver, spleen and brain showed significant increases in SOD activity and increased SOD-mRNA gene expression. CONCLUSIONS: The natural lipophilic antioxidant trilinolein potentiates the SOD antioxidation defense mechanism and increases gene expression of SOD-mRNA after short-term supplementation in rats.

The itinerary of a vesicle component, Aut7p/Cvt5p, terminates in the yeast vacuole via the autophagy/Cvt pathways.

Aminopeptidase I (API) is delivered to the yeast vacuole by one of two alternative pathways, cytoplasm to vacuole targeting (Cvt) or autophagy, depending on nutrient conditions. Genetic, morphological, and biochemical studies indicate that the two pathways share many of the same molecular components. The Cvt pathway functions during vegetative growth, while autophagy is induced during starvation. Both pathways involve the formation of cytosolic vesicles that fuse with the vacuole. In either case, the mechanism of vesicle formation is not known. Autophagic uptake displays a greater capacity for cytosolic protein sequestration. This suggests the involvement of an inducible protein(s) that allows the vesicle-forming machinery to adapt to the increased degradative needs of the cell. We have analyzed the biosynthesis of Aut7p, a protein required for both pathways. We find Aut7p expression is induced by nitrogen starvation. Aut7p is degraded by a process dependent on both proteinase A and Cvt/autophagy components. Protease accessibility assays demonstrate that Aut7p is located within vesicles in strains defective in vesicle delivery or breakdown. Finally, the aut7/cvt5 mutant accumulates precursor API at a stage prior to vesicle completion. These data suggest that Aut7p is induced during autophagy and delivered to the vacuole together with precursor API by Cvt/autophagic vesicles.

Apg9p/Cvt7p is an integral membrane protein required for transport vesicle formation in the Cvt and autophagy pathways.

In nutrient-rich, vegetative conditions, the yeast Saccharomyces cerevisiae transports a resident protease, aminopeptidase I (API), to the vacuole by the cytoplasm to vacuole targeting (Cvt) pathway, thus contributing to the degradative capacity of this organelle. When cells subsequently encounter starvation conditions, the machinery that recruited precursor API (prAPI) also sequesters bulk cytosol for delivery, breakdown, and recycling in the vacuole by the autophagy pathway. Each of these overlapping alternative transport pathways is specifically mobilized depending on environmental cues. The basic mechanism of cargo packaging and delivery involves the formation of a double-membrane transport vesicle around prAPI and/or bulk cytosol. Upon completion, these Cvt and autophagic vesicles are targeted to the vacuole to allow delivery of their lumenal contents. Key questions remain regarding the origin and formation of the transport vesicle. In this study, we have cloned the APG9/CVT7 gene and characterized the gene product. Apg9p/Cvt7p is the first characterized integral membrane protein required for Cvt and autophagy transport. Biochemical and morphological analyses indicate that Apg9p/Cvt7p is localized to large perivacuolar punctate structures, but does not colocalize with typical endomembrane marker proteins. Finally, we have isolated a temperature conditional allele of APG9/CVT7 and demonstrate the direct role of Apg9p/Cvt7p in the formation of the Cvt and autophagic vesicles. From these results, we propose that Apg9p/Cvt7p may serve as a marker for a specialized compartment essential for these vesicle-mediated alternative targeting pathways.

The effect of stevioside on blood pressure and plasma catecholamines in spontaneously hypertensive rats.

Stevioside is a sweet-tasting glycoside, composed of stevia, a diterpenic carboxylic alcohol with three glucose molecules, mainly used as a substitute for non-alcoholic sweetener. It has previously been shown to reduce blood pressure in studies in animals and human. The effect of intravenous stevioside on the blood pressure was studied in spontaneously hypertensive rats (SHR). The hypotensive effect on both systolic and diastolic blood pressure was dose-dependent for intravenous doses of 50, 100 and 200 mg/kg in conscious SHR. The maximum reductions in systolic and diastolic blood pressure were 31.4 +/- 4.2% and 40.8 +/- 5.6% (mean +/- SEM) respectively and the hypotensive effect lasted for more than 60 min with a dose of 200 mg/kg. Serum dopamine, norepinephrine and epinephrine levels were not changed significantly 60 min after intravenous injection of stevioside 100 mg/kg in anesthetized SHR. The present data show that stevioside given intravenously to conscious SHR was effective in blood pressure reduction and there was no change in serum catecholamines in anaesthetized animals with this natural compound.

Randomized, double-blind, placebo-controlled study of the safety and efficacy of vitamin B complex in the treatment of nocturnal leg cramps in elderly patients with hypertension.

Nocturnal leg cramps is a common and troublesome problem in elderly individuals, and their etiology is unknown. Treatment with quinine is a common practice, but the effectiveness of the drug is doubtful and adverse drug effects are common. This randomized, double-blind, placebo-controlled study was conducted to evaluate the safety and efficacy of vitamin B complex capsules (fursulthiamine 50 mg, hydroxocobalamin 250 micrograms, pyridoxal phosphate 30 mg, and riboflavin 5 mg) in 28 elderly patients with hypertension who had severe nocturnal leg cramps that disturbed their sleep. Self-reported ratings of leg cramp frequency, duration, and intensity were used to evaluate severity of nocturnal leg cramps. Both the patients taking vitamin B capsules (n = 14) and those taking placebo (n = 14) received medications three times daily, and were examined regularly at 2-week intervals for 3 months. After 3 months, 86% of the patients taking vitamin B had prominent remission of leg cramps, whereas those taking placebo had no significant difference from baseline. Treatment with vitamin B complex significantly reduced the frequency, intensity, and duration of nocturnal leg cramps. Because quinine is not without potential for side effects, and vitamin B complex is a relatively safe and effective alternative, clinicians should reconsider the treatment of choice for nocturnal leg cramps.

Synthesis of ideal window filter response in grating-assisted couplers.

Synthesizing ideal windowlike spectral response in codirectional grating-assisted couplers is considered. The method of variational optimization is used to design couplers theoretically with near 100% power transfer efficiency over the passband width and with sidelobes suppressed to -40 dB. The physical role of the pi-phase-reversal sections for passband f lattening is explained.

Synthesis of codirectional couplers with ultralow sidelobes and minimum bandwidth.

A general variational optimization procedure is used to synthesize codirectional couplers with arbitrary sidelobe suppression down to -125 dB. Apodization shapes yielding sidelobe levels over the range of -40 dB to -75 dB are given by a single design formula. The limiting performance in terms of sidelobe suppression versus the bandwidth of passive evanescent-type couplers is found.

Polarization corrections of dispersion characteristics of optical waveguides.

The polarization corrections to optical waveguide dispersion characteristics from the scalar wave equations are calculated by an improved perturbation formula and a vector variational expression. More-accurate predictions than with the conventional first-order perturbation theory are demonstrated.

Coupled-mode formulations.

Vector coupled-mode theory is extended beyond the conventional first-order treatment. Good results are obtained from the extended theory in the case of waveguides with large index discontinuity.