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Rhenium disulfide (ReS2) with low structural symmetry and highly spontaneous, exhibits some unique optical and electrical anisotropy properties for developing optoelectronic devices. This work studies the hydrothermal synthesis and the excitonic effects in the linear and nonlinear optical properties of 1T′ phase ReS2. The growth is controlled by adjusting experimental conditions, and its growth mechanism is revealed. The varying degrees of Re vacancy are characterized. They cause the growth direction of ReS2 nanosheets from lateral to agglomeration and the stacks into self‐assembly micro‐nanospheres. The density functional theory explains the electronic and bonding properties of Re vacancy, where the existent defects reduce the band gap and change the states density. Re vacancy increases the conductivity and results in the metallization of ReS2. The photoluminescence intensity of defect emission peak is negatively correlated with the defect level for the enriching vacancies. However, compared with intrinsic peak, it will increase monotonically with the number of bound excitons in defects. Furthermore, the nonlinear absorption properties are obtained by picosecond Z‐scan technique. By adjusting temperature, different degrees of saturation absorption and reverse saturation absorption characteristics appear due to the vacancy effect. The synthesized ReS2 has broad application in photodetectors and optical devices with optical amplitude limiting. [ABSTRACT FROM AUTHOR]

This research constructs a simple model to illustrate the global supply‐chain (GSC) profit sharing and industrial upgrading mechanism, finding that the average profitability distribution in the different supply‐chain stages is determined by three main conditions: (1) the average product of the labor in the firms at each production stage; (2) the production complexity level of each production stage in the chain; and (3) the ratio of the output elasticity of capital to the output elasticity of labor in each stage. This study also proposes a new industrial upgrading mechanism, the "smile‐curve‐driven supply‐chain upgrading," for supply‐chain firms. Increases in production complexity and level of factor intensity in each production stage are found to be the two essential conditions for the smile‐curve‐driven supply‐chain upgrading. Our static and dynamic panel empirical models, including robustness checks, are both broadly consistent with the theoretical predictions of this paper. [ABSTRACT FROM AUTHOR]

Background: Complete right bundle branch block (CRBBB) is an important predictor of atrial fibrillation (AF) recurrence after pulmonary vein isolation. However, the association between CRBBB and AF development remains unclear. Methods: We performed a retrospective study of 2639 patients (male, n = 1549; female, n = 1090; mean age, 58 ± 13 years). CRBBB was defined as a late R (R′) wave in lead V1 or V2 with a slurred S wave in lead I and/or lead V6 with a prolonged QRS duration (≥120 ms). Results: Among the 2639 patients, CRBBB was detected in 40 patients (1.5%), and the prevalence of AF was 7.4% (196/2639). The proportion of patients with AF and CRBBB was higher than the proportion of patients with AF without CRBBB (22.5% vs. 7.2%; p = 0.001). In the forward multivariate logistic analysis, CRBBB (odds ratio [OR], 3.329; 95% confidence interval [CI], 1.350–8.211; p = 0.009), complete left bundle branch block (OR, 2.209; 95% CI, 1.238–3.940; p = 0.007), age (OR, 1.020; 95% CI, 1.005–1.035; p = 0.009), valvular heart disease (OR, 2.332; 95% CI, 1.531–3.552; p < 0.001), left atrial diameter (OR, 1.133; 95% CI, 1.104–1.163; p < 0.001), left ventricular ejection fraction (OR, 1.023; 95% CI, 1.006–1.041; p = 0.007), and class I or III anti‐arrhythmic drug use (OR, 10.534; 95% CI, 7.090–15.651; p < 0.001) were associated with AF. Conclusion: Complete right bundle branch block was significantly associated with AF development in hospitalized patients with cardiovascular diseases. [ABSTRACT FROM AUTHOR]

ABSTRACT Amyloid β peptide (Aβ) has been thought to be neurotoxic and responsible for the impairment of learning and memory in Alzheimer's disease (AD). Humanin (HN), a 24 amino acid polypeptide first identified from the unaffected occipital lobe of an AD patient, is believed to be neuroprotective against the AD-related neurotoxicity. In this study, we investigated the neuroprotective effects of Colivelin (CLN), a novel HN derivative, against Aβ by using behavioral test, in vivo electrophysiological recording, and intracellular calcium imaging. Our results showed that intrahippocampal injection of CLN (0.2 nmol) effectively prevented Aβ25-35 (4 nmol)-induced deficits in spatial learning and memory of rats in Morris water maze test; the suppression of in vivo hippocampal long term potentiation (LTP) by Aβ25-35 was nearly completely prevented by CLN; in addition, CLN pretreatment also effectively inhibited Aβ25-35-induced calcium overload in primary cultured hippocampal neurons. These results indicate that CLN has significant neuroprotective properties against Aβ, and CLN may holds great promise for the treatment and prevention of AD. © 2014 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

ABSTRACT Rattin, a specific derivative of humanin in rats, shares the ability with HN to protect neurons against amyloid β (Aβ) peptide-induced cellular toxicity. However, it is still unclear whether Rattin can protect against Aβ-induced deficits in cognition and synaptic plasticity in rats. In the present study, we observed the effects of Rattin and Aβ31-35 on the spatial reference memory and in vivo hippocampal Long-term potentiation of rats by using Morris water maze test and hippocampal field potential recording. Furthermore, the probable molecular mechanism underlying the neuroprotective roles of Rattin was investigated. We showed that intra-hippocampal injection of Rattin effectively prevented the Aβ31-35-induced spatial memory deficits and hippocampal LTP suppression in rats; the Aβ31-35-induced activation of Caspase-3 and inhibition of STAT3 in the hippocampus were also prevented by Rattin treatment. These findings indicate that Rattin treatment can protect spatial memory and synaptic plasticity of rats against Aβ31-35-induced impairments, and the underlying protective mechanism of Rattin may be involved in STAT3 and Caspases-3 pathways. Therefore, application of Rattin or activation of its signaling pathways in the brain might be beneficial to the prevention of Aβ-related cognitive deficits. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

ABSTRACT Alzheimer's disease (AD), the most prevalent neurodegenerative disease in the elderly, leads to progressive loss of memory and cognitive deficits. Amyloid-β protein (Aβ) in the brain is thought to be the main cause of memory loss in AD. Melatonin, an indole hormone secreted by the pineal gland, has been reported to produce neuroprotective effects. We examined whether melatonin could protect Aβ-induced impairments of hippocampal synaptic plasticity, neuronal cooperative activity, and learning and memory. Rats received bilateral intrahippocampal injection of Aβ1-42 or Aβ31-35 followed by intraperitoneal application of melatonin for 10 days, and the effects of chronic melatonin treatment on in vivo hippocampal long-term potentiation (LTP) and theta rhythm and Morris water maze performance were examined. We showed that intrahippocampal injection of Aβ1-42 or Aβ31-35 impaired hippocampal LTP in vivo, while chronic melatonin treatment reversed Aβ1-42- or Aβ31-35-induced impairments in LTP induction. Intrahippocampal injection of Aβ31-35 impaired spatial learning and decreased the power of theta rhythm in the CA1 region induced by tail pinch, and these synaptic, circuit, and learning deficits were rescued by chronic melatonin treatment. These results provide evidence for the neuroprotective action of melatonin against Aβ insults and suggest a strategy for alleviating cognition deficits of AD. Synapse 67:626-636, 2013. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]