[Show abstract][Hide abstract] ABSTRACT: Several Late Ordovician (late Katian) reef complexes are known from the border area of Jiangxi and Zhejiang provinces in southeast China. We studied two coral–stromatoporoid reefs exposed in the Xiazhen Formation at Zhuzhai (Yushan, Jiangxi). The reefs have a combined thickness of 7.4 m and are metazoan-dominated with most reef-builders in growth position. Stromatoporoids and tabulate corals constitute the framework of the reefs. Stromatoporoids (mostly Clathrodictyon) dominate the first unit and show a vertical increase in proportion and dominance from the middle part to the top of the unit, whereas tabulate corals (dominated by Catenipora and Agetolites) are the main reef-builders in the second unit where stromatoporoids are rare. We attribute this change to a greater tolerance of tabulate corals to turbidity, allowing them to thrive in the muddy facies of the upper unit. This facies change is probably related to the increasing terrestrial input from the northwestward expansion of the Cathaysian Land during the late Katian. The Cathaysian orogeny also led to a short-term exposure of the sea floor in the study area, which terminated the reef growth.
Estonian Journal of Earth Sciences 03/2015; 64(1):68-73. · 0.82 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To investigate whether microRNAs (miRs) can serve as novel biomarkers for in-stent restenosis (ISR).
This retrospective, observational single-centre study was conducted at the cardiovascular department of a tertiary hospital centre in the north of China. Follow-up coronary angiography at 6 to 12 months was performed in 181 consecutive patients implanted with drug-eluting stents. Fifty-two healthy volunteers served as the control group. The plasma miRs levels were analyzed by quantitative real-time PCR. Receiver-operating characteristic curve (ROC) analysis was performed to investigate the characters of these miRs as potential biomarkers of ISR.
MiR-21 levels in ISR patients were significantly higher than those in non-ISR patients and healthy controls (P<0.05), while miR-100 (P<0.05), miR-143 (P<0.001) and miR-145 (P<0.0001) levels were significantly decreased in ISR patients. Further analysis showed that miR-21 levels were remarkably increased (P = 0.045), while miR-100 (P = 0.041), miR-143 (P = 0.029) and miR-145 (P<0.01) levels were dramatically decreased in patients with diffuse ISR compared to those with focal ISR. ROC analysis demonstrated that the area under curve of miR-145, miR-143, miR-100 and miR-21 were 0.880 (95% confidence interval; CI = 0.791-0.987, P<0.001), 0.818 (95% confidence interval; CI = 0.755-0.963, P<0.001), 0.608 (95% confidence interval; CI = 0.372-0.757, P<0.05) and 0.568 (95% confidence interval; CI = 0.372-0.757, P<0.05), with specificity of 83.1%, 80.1%, 68.9% and 68.6%, and sensitivity of 88.7%, 82.1%, 60.2% and 50.1%, respectively.
Circulating miR-143 and miR-145 levels are associated with the occurrence of ISR and can serve as novel noninvasive biomarkers for ISR.
PLoS ONE 11/2014; 9(11):e112043. · 3.53 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Obstructive sleep apnea (OSA) is closely related to atrial fibrillation (AF). However, the roles and mechanisms of chronic OSA in atrial remodeling are still unclear. Canine model of chronic OSA was simulated by stopping the ventilator and closing the airway for 4 h per day and lasting for 12 weeks. AF inducibility and duration was increased while atrial effective refractory period (AERP) was shortened after chronic apnea. Meanwhile, upregulation of proteins encoding inward rectifier K(+) current (I K1), delayed rectifier K(+) current (I Kr and I Ks), acetylcholine activated K(+) current (I KACh), transient outward K(+) current (I to) and ultra-rapid delayed rectifier potassium current (I Kur) as well as downregulation of protein encoding L-type Ca(2+) current (I Ca,L) were found after chronic OSA. Besides abnormal electrical activity, chronic OSA induced apoptosis and interstitial fibrosis of atrial myocytes, which was partly mediated by caspase 9, phosphorylation of extracellular-regulated kinase 1/2, and α-smooth muscle actin. In addition, atrial sympathetic and parasympathetic hyperinnervation were found manifesting by enhanced growth-associated protein 43, tyrosine hydroxylase and elevated choline acetyltransferase. Moreover, protein expression of β1, β2, and M2 receptor were markedly increased by chronic OSA. In summary, we firstly demonstrated in canine model that chronic OSA could shorten AERP and lead to altered expression of important channel proteins, moreover, induce atrial structure remodeling by increased atrial apoptosis, fibrosis, and autonomic remodeling, eventually promoting the development of a substrate of AF. Our findings suggested that reversing atrial remodeling might be a potential therapeutic strategy for OSA-induced AF.
Archiv für Kreislaufforschung 09/2014; 109(5):427. · 5.96 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Early Ordovician (late Tremadocian to early Floian) reefs on the Yangtze Platform margin of the Hunghuayuan Formation at Zhangzhai section in southeastern Guizhou, South China show three types of reefs in two broad categories: microbial-dominated (stromatolite and lithistid sponge-Calathium-calcimicrobial) reefs and metazoan-dominated (lithistid sponge-Calathium) reefs. These reef types represent different communities controlled by varying environmental settings. Stromatolites tended to develop in the shallow subtidal zone, whereas unlaminated calcimicrobial mounds and metazoan-dominated reefs thrived at greater depths. This is the first report on metazoan-dominated reefs at the platform margin of the Hunghuayuan Formation.
[Show abstract][Hide abstract] ABSTRACT: After the end-Ordovician mass extinction, reef recovery (size and biotic diversity) took several million years. On the Upper Yangtze Platform, South China Block, the initial reef reconstruction episode is recorded in limestone of middle Aeronian age in northern Guizhou Province. By late Aeronian, reefs were widespread on the Yangtze carbonate platform, today represented by patch reefs cropping out in a 10-km2 large area near Shuibatang, Tongzi County, where two stratigraphic intervals with reefs are recognized. Late Aeronian reefs constitute a complex and diverse reef community dominated by corals, and to a lesser extent stromatoporoids. They contain an accessory fauna of abundant bryozoans and crinoids and some brachiopods, trilobites, molluscs and calcimicrobes. These reefs correlate in time with similar reefs in Anticosti, Laurentia, palaeogeographically very distant from South China. Thus, there is good evidence that recovery and geographic expansion of reefs after the end-Ordovician extinction occur simultaneously in at least two continents.
[Show abstract][Hide abstract] ABSTRACT: Erythropoietin (EPO) and granulocyte colony-stimulating factor (G-CSF) are both potential novel therapeutics for use after myocardial infarction (MI). However, their underlying mechanisms remain unclear and the efficacy of monotherapy with EPO or G-CSF is also controversial. Therefore, we investigated the effects of combined treatment with EPO and G-CSF on neovascularization and cardiac function in post-infarction rats and explored the potential mechanisms.
Four groups of rats were used: control (saline injection after MI, i.h.), EPO (a single dose of 5 000 IU/kg after MI, i.h.), G-CSF (a dose of 50 µg× kg(-1)× d(-1) for 5 days after MI, i.h.), and both EPO and G-CSF (EPO+G-CSF, using the same regiment as above). Cardiac function was assessed by echocardiography before and 1 day, 7 days, 14 days and 21 days after MI. CD34(+)/Flk-1(+) cells in the peripheral blood were evaluated by flow cytometry before and 3 days, 5 days and 7 days after MI. The infarct area and angiogenesis in the peri-infarct area were analyzed. The mRNA and protein expression of vascular endothelial growth factor (VEGF) and stromal-derived factor-1a (SDF-1α) in the peri-infarct area were detected by real-time quantitative RT-PCR and Western blotting.
Compared with the control and monotherapy groups, the EPO+G-CSF group had significantly increased CD34(+)/Flk-1(+) endothelial progenitor cells (EPCs) in the peripheral blood (P < 0.05), up-regulated VEGF and SDF-1α levels in the peri-infarct region (P < 0.05), enhanced capillary density (P < 0.05), reduced infarct size (P < 0.05) and improved cardiac structure and function (P < 0.05). G-CSF alone did not dramatically increase EPCs in the peripheral blood, enhance capillary density in the peri-infarct area or reduce infarct size compared with the control group.
Combined treatment with EPO and G-CSF increased EPCs mobilization, up-regulated VEGF and SDF-1α levels in the post-infarction microenvironment, subsequently enhanced neovascularization in the peri-infarct region and reduced infarct size. All factors contributed to its beneficial effects on cardiac function in post-infarction rats.
Chinese medical journal 05/2014; 127(9):1677-83. · 1.02 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Reefs in the Late Ordovician are usually built up by metazoans, whereas in the Early and Middle Ordovician microbial reefs are dominating. In the Late Ordovician (Katian) Lianglitag Formation, at Bachu, Tarim, NW China, however, three distinct stages of thrombolithic microbial reefs are exposed. The lower and upper reef intervals are characterized by widespread microbial carbonates with almost constant thicknesses (biostromes). The middle reef interval exposes dome-like mounds, and shows a higher diversity of reef-building and reef-dwelling organisms. Calcareous algae such as Vermiporella are abundant, but also other components such as fragments of Halysis, brachiopods, molluscs, echinoderms, bryozoans, and trilobites have been found in the microbial reef units. The purpose of this study is to describe for the first time the composition and microfacies of the reefs in this remote area. Especially the question of whether or not these Late Ordovician reefs represent remnants of the Early/Middle Ordovician microbial-dominated reef type just lacking Calathium and lithistid sponge is addressed. The results indicate that the local conditions on the leeward side of the carbonate platform, where waters are less well agitated and thus less well oxygenated, and probably also characterized by temporarily elevated water temperatures hampering the growth of metazoan reefs, were responsible for the proliferation of the Late Ordovician microbial reefs in the Bachu area.
[Show abstract][Hide abstract] ABSTRACT: Balloon crossing failure after passing a guidewire usually leads to unsuccessful percutaneous recanalization of chronic total occlusions (CTOs). We sought to investigate a novel technique for solving this problem.
Twenty-one patients with failed balloon crossing through CTOs after successful guidewire passing were treated with the "seesaw balloon-wire cutting" technique between July 2012 and May 2013. The main process of this technique was to insert two guidewires (guidewire A and guidewire B) into the distal true lumen of CTOs and then to advance two short and lowprofile balloons (balloon A and balloon B) over the two guidewires, respectively. Balloon A was first advanced over guidewire A as distally as possible, and then was inflated with high pressure (≥18 atm) to press guidewire B, producing a cutting power to crush the proximal fibrous cap of the CTO. Subsequently, balloon A was withdrawn slightly, and balloon B was advanced as distally as possible and then was inflated to press guidewire A, producing a similar cutting effect to crush the proximal fibrous cap on the other side. The two balloons were progressed alternatively until one of them was able to cross through the occluded segment.
This new technique was successfully applied in 17 patients (81.0%), leading to procedural success of their CTOs. The technique failed in 4 patients (19.0%) due to heavy calcification. No complications occurred in all patients.
The seesaw balloon-wire cutting technique is an effective and safe approach to facilitate balloon crossing during CTO interventions.
The Journal of invasive cardiology 04/2014; 26(4):167-70. · 1.57 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: ANRIL has long been considered as the strongest candidate gene at the 9p21 locus, robustly associated with stroke and coronary artery disease. However, the underlying molecular mechanism remains unknown. The present study works to elucidate such a mechanism.
Using expression quantitative loci analysis, we identified potential genes whose expression may be influenced by genetic variation in ANRIL. To verify the identified gene(s), knockdown and overexpression of ANRIL were evaluated in human umbilical vein endothelial cells and HepG2 cells. Ischemic stroke and coronary artery disease risk were then evaluated in the gene(s) demonstrated to be mediated by ANRIL in 3 populations of Chinese Han ancestry: 2 ischemic stroke populations consisting of the Central China cohort (903 cases and 873 controls) and the Northern China cohort (816 cases and 879 controls) and 1 coronary artery disease cohort consisting of 772 patients and 873 controls.
Expression quantitative loci analysis identified CARD8 among others, with knockdown of ANRIL expression decreasing CARD8 expression and overexpression of ANRIL increasing CARD8 expression. The minor T allele of a previously identified CARD8 variant (rs2043211) was found to be significantly associated with a protective effect of ischemic stroke under the recessive model in 2 independent stroke cohorts. No significant association was found between rs2043211 and coronary artery disease.
CARD8 is a downstream target gene regulated by ANRIL. Single nucleotide polymorphism rs2043211 in CARD8 is significantly associated with ischemic stroke. ANRIL may increase the risk of ischemic stroke through regulation of the CARD8 pathway.
[Show abstract][Hide abstract] ABSTRACT: The effects of interleukin-33 (IL-33) on the immune system have been clearly demonstrated; however, in cardiovascular diseases, especially in coronary artery disease (CAD), these effects have not yet been clarified. In this study, we investigate the genetic role of the IL-33-ST2L pathway in CAD. We performed three-stage case-control association analyses on a total of 4,521 individuals with CAD and 4,809 controls via tag SNPs in the genes encoding IL-33 and ST2L-IL-1RL1. One tag SNP in each gene was significantly associated with CAD (rs7025417(T) in IL33, padj = 1.19 × 10(-28), OR = 1.39, 95% CI: 1.31-1.47; rs11685424(G) in IL1RL1, padj = 6.93 × 10(-30), OR = 1.40, 95% CI: 1.32-1.48). Combining significant variants in two genes, the risk for CAD increased nearly 5-fold (padj = 8.90 × 10(-21), OR = 4.98, 95% CI: 3.56-6.97). Traditional risk factors for CAD were adjusted for the association studies by SPSS with logistic regression analysis. With the two variants above, both located within the gene promoter regions, reporter gene analysis indicated that the rs7025417 C>T and rs11685424 A>G changes resulted in altered regulation of IL33 and IL1RL1 gene expression, respectively (p < 0.005). Further studies revealed that the rs7025417 genotype was significantly associated with plasma IL-33 levels in the detectable subjects (n = 227, R(2) = 0.276, p = 1.77 × 10(-17)): the level of IL-33 protein increased with the number of rs7025417 risk (T) alleles. Based on genetic evidence in humans, the IL-33-ST2L pathway appears to have a causal role in the development of CAD, highlighting this pathway as a valuable target for the prevention and treatment of CAD.
The American Journal of Human Genetics 09/2013; · 11.20 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: A series of pyrrolo[1,2-a]pyrazinone compounds (5a–9f) were synthesized, and their cytotoxic activity against SKOV-3, A549, HeLa cells in vitro were evaluated by the MTT method. Some of the compounds showed potential antitumor activity against three tumor cell lines. Among them, compounds 9c and 9d showed the most potent cytotoxic activity. The preliminary mechanism of action was discussed.
Chinese Chemical Letters 07/2013; 24(7):619–621. · 1.18 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Hepatitis C virus (HCV) nonstructural protein 5A (NS5A) is a remarkable protein as it clearly plays multiple roles in mediating viral replication, host-cell interactions and viral pathogenesis. However, on the impact of cell growth, there have been different study results. NS5ATP9, also known as KIAA0101, p15PAF, L5, and OEACT-1, was first identified as a proliferating cell nuclear antigen-binding protein. Earlier studies have shown that NS5ATP9 might play an important role in HCV infection. The aim of this study is to investigate the function of NS5ATP9 on hepatocellular carcinoma (HCC) cell lines proliferation under HCV NS5A expression. The results showed that overexpression of NS5ATP9 inhibited the proliferation of Bel7402 cells, whereas knockdown of NS5ATP9 by interfering RNA promoted the growth of HepG2 cells. Under HCV NS5A expression, RNA interference (RNAi) targeting of NS5ATP9 could reverse the inhibition of HepG2 cell proliferation, suggesting that NS5ATP9 might be an anti-proliferation gene that plays an important role in the suppression of cell growth mediated by HCV NS5A via MEK/ERK signaling pathway. These findings might provide new insights into HCV NS5A and NS5ATP9.
International Journal of Molecular Sciences 05/2013; 14(5):10539-10551. · 2.34 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Atrial fibrillation (AF) is a highly prevalent arrhythmia with pronounced morbidity and mortality. Inward-rectifier K+ current (IK1) is believed to be an important regulator of reentrant-spiral dynamics and a major component of AF-related electrical remodeling. MicroRNA-26 (miR-26) is predicted to target the gene encoding KIR2.1, KCNJ2. We found that miR-26 was downregulated in atrial samples from AF animals and patients and this downregulation was accompanied by upregulation of IK1/KIR2.1 protein. miR-26 overexpression suppressed expression of KCNJ2/KIR2.1. In contrast, miR-26 knockdown, inhibition, or binding-site mutation enhanced KCNJ2/KIR2.1 expression, establishing KCNJ2 as a miR-26 target. Knockdown of endogenous miR-26 promoted AF in mice, whereas adenovirus-mediated expression of miR-26 reduced AF vulnerability. Kcnj2-specific miR-masks eliminated miR-26-mediated reductions in Kcnj2, abolishing miR-26's protective effects, while coinjection of a Kcnj2-specific miR-mimic prevented miR-26 knockdown-associated AF in mice. Nuclear factor of activated T cells (NFAT), a known actor in AF-associated remodeling, was found to negatively regulate miR-26 transcription. Our results demonstrate that miR-26 controls the expression of KCNJ2 and suggest that this downregulation may promote AF.
The Journal of clinical investigation 04/2013; · 15.39 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: FUZHENGHUAYU Tablets have been widely used in the treatment of liver fibrosis in China. Here, we investigate the apoptotic effect of FUZHENGHUAYU Tablet in rat liver stellate cell line HSC-T6. HSC-T6 cells were incubated with control serum or drug serum from rats fed with 0.9% NaCl or FUZHENGHUAYU Tablet, respectively. Cells exposed to drug serum showed higher proportions of early and late apoptotic cells than controls. The mRNA levels of collagens I and III, TGF-β1 and α-SMA were reduced by drug serum compared to control serum. Differentially expressed mRNAs and miRNAs were analyzed by microarray and sequencing, respectively. We identified 334 differentially expressed mRNAs and also 60 GOs and two pathways related to the mRNAs. Seventy-five differentially expressed miRNAs were down-regulated by drug serum and 1963 target genes were predicted. 134 GOs up-regulated in drug serum group were linked to miRNA targets, and drug serum also regulated 43 miRNA signal transduction pathways. Protein levels were evaluated by Western blot. Drug serum down-regulated (phospho-SAPK/JNK)/(SAPK/JNK) and up-regulated phospho-p38/p38 ratios. The study showed that FUZHENGHUAYU Tablet induced apoptosis in rat HSC-T6 cells possibly in part by activating p38 and inhibiting SAPK/JNK.
Evidence-based Complementary and Alternative Medicine 01/2013; 2013:368103. · 2.18 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Identifying the key factor mediating pathological cardiac hypertrophy is critically important for developing the strategy to protect against heart failure. Bone morphogenetic protein-4 (BMP4) is a mechanosensitive and proinflammatory gene. In this study, we investigated the role of BMP4 in cardiac hypertrophy, apoptosis, and fibrosis in experimentally pathological cardiac hypertrophy. The in vivo pathological cardiac hypertrophy models were induced by pressure-overload and angiotensin (Ang) II constant infusion in mice, and the in vitro model was induced by Ang II exposure to cultured cardiomyocytes. The expression of BMP4 increased in pressure overload, Ang II constant infusion-induced pathological cardiac hypertrophy, but not in swimming exercise-induced physiological cardiac hypertrophy in mice. BMP4 expression also increased in Ang II-induced cardiomyocyte hypertrophy in vitro. In turn, BMP4 induced cardiomyocyte hypertrophy, apoptosis, and cardiac fibrosis, and these pathological consequences were inhibited by the treatment with BMP4 inhibitors noggin and DMH1. Moreover, Ang II-induced cardiomyocyte hypertrophy was inhibited by BMP4 inhibitors. The underlying mechanism that BMP4-induced cardiomyocyte hypertrophy and apoptosis was through increasing NADPH oxidase 4 expression and reactive oxygen species-dependent pathways. Lentivirus-mediated overexpression of BMP4 recapitulated hypertrophy and apoptosis in cultured cardiomyocytes. BMP4 inhibitor DMH1 inhibited pressure overload-induced cardiac hypertrophy in mice in vivo. The plasma BMP4 level of heart failure patients was increased compared with that of subjects without heart failure. In summary, we conclude that BMP4 is a mediator and novel therapeutic target for pathological cardiac hypertrophy.