Modal identification of civil structures via covariance-driven stochastic subspace method.

It is usually of great importance to identify modal parameters for dynamic analysis and vibration control of civil structures. Unlike the cases in many other fields such as mechanical engineering where the input excitation of a dynamic system may be well quantified, those in civil engineering are commonly characterized by unknown external forces. During the last two decades, stochastic subspace identification (SSI) method has been developed as an advanced modal identification technique which is driven by output-only records. This method combines the theory of system identification, linear algebra (e.g., singular value decomposition) and statistics. Through matrix calculation, the so-called system matrix can be identified, from which the modal parameters can be determined. The SSI method can identify not only the natural frequencies but also the modal shapes and damping ratios associated with multiple modes of the system simultaneously, making it of particular efficiency. In this study, main steps involved in the modal identification process via the covariance-driven SSI method are introduced first. A case study is then presented to demonstrate the accuracy and efficiency of this method, through comparing the corresponding results with those via an alternative method. The effects of noise contaminated in output signals on identification results are stressed. Special attention is also paid to how to determine the mode order accurately.

Protective effects of parecoxib on rat primary astrocytes from oxidative stress induced by hydrogen peroxide.

OBJECTIVE: To investigate the protective effects of parecoxib from oxidative stress induced by hydrogen peroxide (H2O2) in rat astrocytes in vitro. METHODS: All experiments included 4 groups: (1) negative control (NC) group, without any treatment; (2) H2O2 treatment group, 100 µmol/L H2O2 treatment for 24 h; (3) and (4) parecoxib pretreatment groups, 80 and 160 µmol/L parecoxib treatment for 24 h, respectively, and then treated with 100 µmol/L H2O2. Several indices were investigated, and the expressions of Bax, Bcl-2, and brain-derived neurotrophic factor (BDNF) were quantified. RESULTS: Compared to the NC group, exposure to H2O2 resulted in significant morphological changes, which could be reversed by pretreatment of parecoxib. In addition, H2O2 treatment led to loss of viability (P=0.026) and increased intracellular reactive oxygen species (ROS) levels (P<0.001), and induced apoptosis (P<0.01) in the primary astrocytes relative to the NC group. However, in the parecoxib pretreatment groups, all the above changes reversed significantly (P<0.05) as compared to the H2O2 treatment group, and were nearly unchanged when compared to the NC group. Mechanical investigation showed that dysregulated Bax, Bcl-2, and BDNF could be implicated in these changes. CONCLUSIONS: Our results indicated that parecoxib provided a protective effect from oxidative stress induced by exposure to H2O2.

Decreased PSD95 expression in medial prefrontal cortex (mPFC) was associated with cognitive impairment induced by sevoflurane anesthesia.

OBJECTIVE: Though sevoflurane has been widely used as an anesthetic in surgery, recent studies have shown that exposure to sevoflurane alone could lead to postoperative cognitive dysfunction (POCD), of which the mechanisms still remain largely unknown. The medial prefrontal cortex (mPFC) is known to be implicated in various cognitive impairments, including working memory and attentional processes. In the present study, we tried to identify dysregulated gene expression in mPFC and investigate the underlying mechanisms involved in POCD. METHODS: Behavioral tests, including elevated plus-maze, O-maze, and Y-maze tests, were performed on Wistar rats exposed to sevoflurane. Whole-genome mRNA profiling of mPFC from Wistar rats after exposure to sevoflurane was carried out. Real-time polymerase chain reaction (PCR) was done to verify the differentially expressed genes. RESULTS: Significant impairment of working memory of rats after exposure to sevoflurane was observed. A total of 119 of 7319 detected mRNAs showed significantly different expression between rats with and without sevoflurane exposure (fold change (FC)>2.0, P<0.05, and false discovery rate (FDR)<0.05), among which 74 mRNAs were down-regulated and 45 mRNAs were up-regulated. Postsynaptic density-95 (PSD95, also named DLG4) showed the most significantly decreased expression in mPFC and further investigation indicated that PSD95 expression level was correlated with spatial working memory performance. CONCLUSIONS: Our study revealed that PSD95 might be involved in the mechanism of POCD, which could provide clues for preventing POCD in clinical operations.

Magnesium sulfate enhances non-depolarizing muscle relaxant vecuronium action at adult muscle-type nicotinic acetylcholine receptor in vitro.

AIM: To investigate the effect of magnesium sulfate and its interaction with the non-depolarizing muscle relaxant vecuronium at adult muscle-type acetylcholine receptors in vitro. METHODS: Adult muscle-type acetylcholine receptors were expressed in HEK293 cells. Drug-containing solution was applied via a gravity-driven perfusion system. The inward currents were activated by brief application of acetylcholine (ACh), and recorded using whole-cell voltage-clamp technique. RESULTS: Magnesium sulfate (1-100 mmol/L) inhibited the inward currents induced ACh (10 µmol/L) in a concentration-dependent manner (IC(50)=29.2 mmol/L). The inhibition of magnesium sulfate was non-competitive. In contrast, vecuronium produced a potent inhibition on the adult muscle-type acetylcholine receptor (IC(50)=8.7 nmol/L) by competitive antagonism. Magnesium sulfate at the concentrations of 1, 3, and 6 mmol/L markedly enhanced the inhibition of vecuronium (10 nmol/L) on adult muscle-type acetylcholine receptors. CONCLUSION: Clinical enhancement of vecuronium-induced muscle relaxation by magnesium sulfate can be attributed partly to synergism between magnesium sulfate and non-depolarizing muscle relaxants at adult muscle-type acetylcholine receptors.