Forward-looking Disclosure and Corporate Governance Characteristics: Evidence from China.

This paper investigates the relationship between forward-looking disclosure (FLD) and a range of corporate governance characteristics in the Chinese stock markets. It finds that the implementation of certain monitoring and control mechanisms, such as independent directors on the board of directors, can improve the extent of FLD. However, separating the roles of the CEO and the chairman of the board of directors is of little help in explaining any improvement in FLD. In contrast, ownership structure appears to play an essential role in determining FLD policies. Indeed, listed firms with high levels of foreign ownership tend to disclose more forward-looking information. Of particular interest, the association between state ownership and FLD is likely to be non-linear, and the inflection point at which the association becomes negative occurs at a state ownership over 38%. In summary, this study provides new evidence on the impact of FLD on corporate governance characteristics on in China’s unique institutional environment. Keywords: Forward-looking Disclosure, Corporate Governance Characteristics, Firm Characteristics, Information Asymmetry, and Chin

NMDA receptor internalization down-regulates NMDA receptor-mediated synaptic responses through the inhibition of remaining (non-internalized) surface NMDA receptors

Cell-surface protein endocytosis is critically involved in the regulation of organismal homeostasis, immune responses, development and neurotransmission [1,2,3,4]. Mechanisms underlying the endocytosis of cell surface proteins have been extensively investigated. However, until very recently no study has reported how non-internalized cell surface proteins may behave following endocytosis of same type of proteins. Here, we highlight findings that regulated NMDA receptor (NMDAR) internalization not only reduces the amount of NMDARs expressed on neuronal surface but also through activating PKD1 pathway phosphorylates and down-regulates remaining (non-internalized) surface NMDARs. This down-regulation of remaining surface NMDARs plays a critical role in the modulation of NMDAR-mediated synaptic responses by NMDAR internalization

Variational-based data assimilation to simulate sediment concentration in the Lower Yellow River, China

The heavy sediment load of the Yellow River makes it difficult to simulate sediment concentration using classic numerical models. In this paper, on the basis of the classic one-dimensional numerical model of open channel flow, a variational-based data assimilation method is introduced to improve the simulation accuracy of sediment concentration and to estimate parameters in sediment carrying capacity. In this method, a cost function is introduced first to determine the difference between the sediment concentration distributions and available field observations. A one-dimensional suspended sediment transport equation, assumed as a constraint, is integrated into the cost function. An adjoint equation of the data assimilation system is used to solve the minimum problem of the cost function. Field data observed from the Yellow River in 2013 are used to test the proposed method. When running the numerical model with the data assimilation method, errors between the calculations and the observations are analyzed. Results show that (1) the data assimilation system can improve the prediction accuracy of suspended sediment concentration; (2) the variational inverse data assimilation is an effective way to estimate the model parameters, which are poorly known in previous research; and (3) although the available observations are limited to two cross sections located in the central portion of the study reach, the variational-based data assimilation system has a positive effect on the simulated results in the portion of the model domain in which no observations are available

A turn-off fluorescent probe for the detection of Cu2+ based on a tetraphenylethylene-functionalized salicylaldehyde Schiff-base

A non-planar tetraphenylethylene-functionalized salicylaldehyde Schiff-base fluorescent probe (TPE-An-Py) with aggregation-induced enhanced emission (AIEE) characteristics was synthesized via a classical Knoevenagel condensation reaction, and exhibited a high sensitivity towards copper ions in aqueous media with a "turn-off" fluorescence mechanism; the limit of detection is 2.36 × 10-7 mol L-1. Importantly, the coordination mode of the probe towards copper was further evaluated by UV-vis and NMR spectroscopy and a 1:2 stoichiometry was identified. A single crystal X-ray diffraction study confirmed the binding mode. In addition, the AIEE fluorescent probe can be applied to the detection of Cu2+ in practical samples with satisfactory recoveries in a range of 106-111% in lake water and 97-108% in tap water

The Role of Chaperone-Mediated Autophagy in Huntingtin Degradation

Huntington Disease (HD) is caused by an abnormal expansion of polyQ tract in the protein named huntingtin (Htt). HD pathology is featured by accumulation and aggregation of mutant Htt in striatal and cortical neurons. Aberrant Htt degradation is implicated in HD pathogenesis. The aim of this study was to investigate the regulatory role of chaperone-mediated autophagy (CMA) components, heat shock protein cognate 70 (Hsc70) and lysosome-associated protein 2A (LAMP-2A) in degradation of Htt fragment 1-552aa (Htt-552). A cell model of HD was produced by overexpression of Htt-552 with adenovirus. The involvement of CMA components in degradation of Htt-552 was determined with over-expression or silencing of Hsc70 and LAMP-2A. The results confirmed previous reports that both macroautophagy and CMA were involved in degradation of Htt-552. Changing the levels of CMA-related proteins affected the accumulation of Htt-552. The lysosomal binding and luminal transport of Htt-552 was demonstrated by incubation of Htt-552 with isolated lysosomes. Expansion of the polyQ tract in Htt-552 impaired its uptake and degradation by lysosomes. Mutation of putative KFERQ motif in wild-type Htt-552 interfered with interactions between Htt-552 and Hsc70. Endogenous Hsc70 and LAMP-2A interacted with exogenously expressed Htt-552. Modulating the levels of CMA related proteins degraded endogenous full-length Htt. These studies suggest that Hsc70 and LAMP-2A through CMA play a role in the clearance of Htt and suggest a novel strategy to target the degradation of mutant Htt

Activation Of Mitochondrial Atp-Sensitive Potassium Channels Improves Rotenone-Related Motor And Neurochemical Alterations In Rats

Our previous studies revealed that activation of mitochondrial ATP-sensitive potassium channels exerted protective effects on rotenone-treated rats and cultured cells. The aim of the present study is to examine the potential therapeutic effects of iptakalim, an ATP-sensitive potassium-channel opener, and diazoxide, a selective mitochondrial ATP-sensitive potassium-channel opener, on Parkinsonian symptoms in rats induced by rotenone. Rats were treated with rotenone (2.5 mg/kg s.c.) daily for 4 wk. This treatment caused a depletion of dopamine in the striatum and substantia nigra. Behaviourally, rotenone-infused rats exhibit Parkinsonian symptoms. Catalepsy was estimated by a 9-cm bar test. Treatment with L-dopa (10 mg/kg.d p.o.), iptakalim (0.75, 1.5, 3.0 mg/kg.d p.o.) and diazoxide (3.0 mg/kg.d p.o.) for 2 wk improved behavioural dysfunction and elevated dopamine contents in the striatum and substantia nigra of rotenone-treated rats. Studies also found that iptakalim and diazoxide could reduce the enzymic activities and mRNA levels of inducible nitric oxide synthase elicited by chronic administration of rotenone. All neurorestorative effects by both iptakalim and diazoxide were abolished by 5-hydroxydecanoate, a selective mitochondrial ATP-sensitive potassium-channel blocker. Collectively, the data suggested that mitochondrial ATP-sensitive potassium channels play a key role in improving both Parkinsonian symptoms and neurochemistry alterations of rotenone model rats, and selective activation of mitochondrial ATP-sensitive potassium channels may provide a new therapeutic strategy for treatment of early Parkinson\u27s disease. Copyright © 2005 CINP