Shandong Provincial Taishan Hospital

Taian, China

Shandong Provincial Taishan Hospital

Taian, China

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Liu S.,Shandong University | Hou Y.,Shandong University | Liu W.,Shandong University | Lu C.,Shandong University | And 2 more authors.
Eukaryotic Cell | Year: 2015

In recent years, the emergence of fungal resistance has become frequent, partly due to the widespread clinical use of fluconazole, which is minimally toxic and effective in the prevention and treatment of Candida albicans infections. The limited selection of antifungal drugs for clinical fungal infection therapy has prompted us to search for new antifungal drug targets. Calcium, which acts as the second messenger in both mammals and fungi, plays a direct role in controlling the expression patterns of its signalling systems and has important roles in cell survival. In addition, calcium and some of the components, mainly calcineurin, in the fungal calcium signaling pathway mediate fungal resistance to antifungal drugs. Therefore, an overview of the components of the fungal calcium-calcineurin signaling network and their potential roles as antifungal targets is urgently needed. The calciumcalcineurin signaling pathway consists of various channels, transporters, pumps, and other proteins or enzymes. Many transcriptional profiles have indicated that mutant strains that lack some of these components are sensitized to fluconazole or other antifungal drugs. In addition, many researchers have identified efficient compounds that exhibit antifungal activity by themselves or in combination with antifungal drugs by targeting some of the components in the fungal calcium-calcineurin signalling pathway. This targeting disrupts Ca2+ homeostasis, which suggests that this pathway contains potential targets for the development of new antifungal drugs. © 2015, American Society for Microbiology. All rights reserved.


Li Z.,Shandong University | Li Z.,Shandong Provincial Taishan Hospital | Wang M.,Shandong University | Wang M.,Peoples Hospital of Liaocheng | And 4 more authors.
PACE - Pacing and Clinical Electrophysiology | Year: 2015

Background The neural remodeling of the atrium plays an important role in the initiation of atrial fibrillation after myocardial infarction (MI); however, the effects of the left stellate ganglion (LSG) on the neural remodeling of the atrium remain incompletely understood. Thus, this study investigated the mechanism by which the LSG mediates sympathetic neural remodeling of the left atrium (LA) in rats after MI. Methods Sixty rats were randomly divided into a Sham group and an MI group. The expression levels of growth-associated protein-43 (GAP43) and nerve growth factor (NGF) messenger ribonucleic acid (mRNA) were measured by reverse transcription polymerase chain reaction. Immunohistochemistry was used to detect the distribution and density of GAP43- and NGF-positive nerves. The expression levels of the proteins were quantified by Western blotting. Results Compared with the Sham group, GAP43 mRNA expression in the LSG was increased in the MI group (P < 0.01), but not significantly increased in the LA. Immunohistochemical analysis demonstrated that in both the LSG and the LA, the mean densities of GAP43- and NGF-positive nerves in the MI group were increased (P < 0.01). In both the LSG and the LA, the protein levels of GAP43 and NGF in the MI group were increased relative to the Sham group (P < 0.01). Conclusions The increased levels of NGF and GAP43 proteins can induce sympathetic nerve hyperinnervation in the LSG and the LA after MI. The increased GAP43 proteins in the LA, which may have been transported from the LSG, accelerated LA sympathetic neural remodeling in rats. © 2014 Wiley Periodicals, Inc.


Wang M.,Shandong University | Wang M.,Peoples Hospital of Liaocheng | Li Z.,Shandong University | Li Z.,Shandong Provincial Taishan Hospital | And 5 more authors.
Heart Lung and Circulation | Year: 2015

Objective: The purpose of this study was to verify the hypothesis that rosuvastatin attenuates atrial structural remodelling in rats with myocardial infarction (MI) through the regulation of the p38 mitogen-activated protein kinase (MAPK) signalling pathway. Methods: A total of 66 rats were used in this study to establish a model of MI. The 56 rats that survived the first 24. h after surgery were randomly divided into four groups: the control group (C group), the rosuvastatin group (R group), the low-dose torasemide group (T1 group), and the high-dose torasemide group (T2 group). The four groups of rats received daily intragastric administration of normal saline, rosuvastatin, or torasemide (T1: 1. mg/kg body weight; T2: 2. mg/kg body weight) for a total of four weeks. The rats in the sham-operated group (n. = 14) also received daily intragastric administration of normal saline for four weeks. After four weeks of intervention, the left ventricular end-diastolic pressure (LVEDP) was measured in all groups of rats by haemodynamic methods. The rats were then sacrificed, and the left atrial tissues were collected. The collagen volume fractions (CVFs) in the left atrial tissues were determined using Masson's trichrome staining. The expression of phosphorylated p38 (P-p38) MAPK in the left atrial tissues was examined by immunohistochemistry and western blot analysis. Results: The results showed that LVEDP, CVF, and P-p38 MAPK expression were drastically elevated in the four MI groups in comparison to the sham-operated group (p. <. 0.001). Rosuvastatin elevated the left ventricular fractional shortening (LVFS) and left ventricular ejection fraction (LVEF). Both rosuvastatin and torasemide improved the haemodynamic parameters. No significant difference was detected in LVEDP between the R group and the T1 group (p. = 0.37). In contrast, LVEDP was significantly higher in the R group than in the T2 group (p <0.05). CVF (%) was markedly decreased in the R group compared to the C, T1, and T2 groups (decreased by 47.4%, 28%, and 20.1%, respectively). Immunohistochemical analysis showed that the indices of P-p38 MAPK positive cells were significantly decreased in the R group in comparison with the C, T1, and T2 groups (decreased by 44.6%, 36.6%, and 21.4%, respectively). Western blot analysis demonstrated that P-p38 MAPK expression was markedly reduced in the R group compared with the C and T1 groups (reduced by 67% and 40.5%, respectively). The level of P-p38 MAPK in the R group was slightly higher than in the T2 group. However, the difference was not statistically significant (p. >. 0.05). Conclusion: Rosuvastatin attenuates atrial structural remodelling in rats with MI. The mechanism underlying this phenomenon may be associated with the downregulation of P-p38 MAPK by rosuvastatin. © 2014 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ).

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