Search

From an industrial waste phenazine, a series of novel redox-active materials were effectively achieved and exploited as sustainable superior organic cathode materials of lithium-ion batteries.

An industrial-waste-derived polymer, PBMEP, was effectively synthesized as a superior sustainable LIB cathode material with robust cycling stability, high working potentials, and excellent rate capability.

Due to their readily availability and high capacity, redox-active small organic molecules have been considered as one of the most promising electrode materials. However, their facile dissolution into organic electrolytes deteriorates their cycle performance, thus limiting the application of organic small molecules as electrode materials. In this study, a novel redox-active molecule, lithium bis(2,3-dihydroxyphenazine) borate (LDPB), was accomplished effectively from 2,3-dihydroxyphenazine (DHP) through a spiroborate salification strategy. When used as lithium storage materials, compared with its precursor DHP, LDPB shows better cycle stability, rate performance, and higher capacity retention (84.6%, after 250 cycles at 200 mA g-1). This spiroborate salification strategy could serve as an efficient approach to construct novel organic electrode material.

We used the mark weighted correlation functions (MCFs), $W(s)$, to study the large scale structure of the Universe. We studied five types of MCFs with the weighting scheme $\rho^\alpha$, where $\rho$ is the local density, and $\alpha$ is taken as $-1,\ -0.5,\ 0,\ 0.5$, and 1. We found that different MCFs have very different amplitudes and scale-dependence. Some of the MCFs exhibit distinctive peaks and valleys that do not exist in the standard correlation functions. Their locations are robust against the redshifts and the background geometry, however it is unlikely that they can be used as ``standard rulers'' to probe the cosmic expansion history. Nonetheless we find that these features may be used to probe parameters related with the structure formation history, such as the values of $\sigma_8$ and the galaxy bias. Finally, after conducting a comprehensive analysis using the full shapes of the $W(s)$s and $W_{\Delta s}(\mu)$s, we found that, combining different types of MCFs can significantly improve the cosmological parameter constraints. Compared with using only the standard correlation function, the combinations of MCFs with $\alpha=0,\ 0.5,\ 1$ and $\alpha=0,\ -1,\ -0.5,\ 0.5,\ 1$ can improve the constraints on $\Omega_m$ and $w$ by $\approx30\%$ and $50\%$, respectively. We find highly significant evidence that MCFs can improve cosmological parameter constraints., Comment: 15pages, 17figures, APJ accepted

Sun W, Wu J, Lin L, Huang Y, Chen Q, Ji Y. Porphyromonas gingivalis stimulates the release of nitric oxide by inducing expression of inducible nitric oxide synthases and inhibiting endothelial nitric oxide synthases. J Periodont Res 2010; 45: 381–388. © 2010 The Authors. Journal compilation © 2010 Blackwell Munksgaard Background and Objective: The purpose of this study was to examine the ability of Porphyromonas gingivalis to invade human umbilical vein endothelial cells (HUVECs) and to study the effects of P. gingivalis ATCC 33277 on the production of nitric oxide (NO) and on the expression of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) in HUVECs. We attempted to throw light on the pathway of damage to endothelial function induced by P. gingivalis ATCC 33277. Material and Methods: P. gingivalis ATCC 33277 was cultured anaerobically, and HUVECs were treated with P. gingivalis ATCC 33277 at multiplicities of infection of 1:10 or 1:100 for 4, 8, 12 and 24 h. HUVECs were observed using an inverted microscope and transmission electron microscopy. NO production was assayed through measuring the accumulation of nitrite in culture supernatants. Expression of both iNOS and eNOS proteins was investigated through western blotting. Results: It was found that P. gingivalis ATCC 33277 can adhere to HUVECs by fimbriae, invade into HUVECs and exist in the cytoplasm and vacuoles. P. gingivalis ATCC 33277 can induce iNOS and inhibit eNOS expression, and stimulate the release of NO without any additional stimulant. Conclusion: Our study provides evidence that P. gingivalis ATCC 33277 can invade HUVECs, and the ability of P. gingivalis ATCC 33277 to promote the production of NO may be important in endothelial dysfunction, suggesting that P. gingivalis ATCC 33277may be one of the pathogens responsible for atherosclerosis.

To investigate whether resveratrol, a polyphenolic compound in red wine, affects the oxidation of human low density lipoprotein (LDL), LDL purified from normolipidemic subjects was subjected to Cu(2+)-induce and azo compound-initiated oxidative modification, with and without the addition of varying concentrations of resveratrol. Modification of LDL was assessed by the formation of thiobarbituric acid reactive substances (TBARS) and changes in the relative electrophoretic mobility (REM) of LDL on agarose gels. Resveratrol (50 microM) reduced TBARS and REM of LDL during Cu(2+)-induced oxidation by 70.5% and 42.3%, respectively (p < 0.01), and prolonged the lag phase associated with the oxidative modification of LDL by copper ion or azo compound. These in vitro results suggest that resveratrol may afford protection of LDL against oxidative damage resulting from exposure to various environmental challenges, possibly by acting as a free radical scavenger.

SUMMARY 1 Resveratrol, a polyphenol in red wine, has a cardioprotective effect. Resveratrol-targeting protein (RTP) has been purified using a resveratrol affinity column (RAC) and has been identified as quinone reductase type 2 (NQO2). We hypothesize that NQO2 is the target protein of resveratrol in vascular smooth muscle cells (VSMC) and that resveratrol inhibits proliferation of VSMC through its action on NQO2. In the present study, we investigated the correlation between NQO2 regulation and cell proliferation in VSMC in response to resveratrol treatment. 2 The RTP was purified using RAC and was detected with a NQO2 polyclonal antibody. The VSMC were incubated with resveratrol (1, 10 and 50 µmol/L) for 24, 48 and 72 h. Cell proliferation was detected by cell counting and bromodeoxyuridine (BrdU) assay. A lentiviral vector incorporating NQO2 short interference (si) RNA of short hairpin design was constructed and transduced into VSMC. Real-time quantitative polymerase chain reactionwas used to measure NQO2 mRNA levels; NQO2 expression was determined by western blot analysis. 3 Using RAC, we extracted a 26 kDa protein from aortic smooth muscle, which was referred to as RTP-26. Proliferation of VSMC was inhibited by resveratrol in a concentration- and time-dependent manner. The mRNA and protein expression of NQO2 was also repressed by resveratrol in a concentration- and time-dependent manner. A similar pattern of inhibition was observed for cells treated with resveratrol (25 µmol/L) as for cells transduced with a lentiviral vector containing siRNA sequences against NQO2. 4 Collectively, these data indicate that the suppression of VSMC proliferation mediated by resveratrol correlates with NQO2 downregulation.

Ventricular tachyarrhythmias are often precipitated by physical or emotional stress, indicating a link between increased adrenergic stimulation and cardiac ion channel activity. Human ether-a-go-go related gene (hERG) potassium channels conduct the rapid component of delayed rectifier potassium current, I(kr), a crucial component for action potential repolarization. To evaluate the correlation between increased alpha(1)-adrenergic activity and the rapid component of cardiac I(kr), whole-cell patch-clamp recording was performed in isolated guinea-pig ventricular myocytes. Stimulation of alpha(1)-adrenoceptors using phenylephrine (0.1 nM-100 microM) reduced I(kr) current in a dose-dependent manner at 37 degrees C. Phenylephrine (0.1 microM) reduced I(kr) current to 66.83+/-3.16%. Chelerythrine (1 microM), a specific inhibitor of protein kinase C (PKC) completely inhibited the changes in I(kr) trigged by 0.1 microM phenylephrine. KT5720 (2.5 microM), a specific inhibitor of protein kinase A (PKA) partially inhibited the current decrease induced by 0.1 microM phenylephrine. Both chelerythrine and KT5720 drastically reduced the phenylephrine-induced effects, indicating possible involvement of PKC and PKA in the alpha(1)-adrenergic inhibition of I(kr). Our data suggest a link between I(kr) and the alpha(1)-adrenoceptor, involving activation of PKC and PKA in arrhythmogenesis.

Ostium secundum atrial septal defect (osASD) is one of the most commonly occurring cardiac malformations. Although some embryological pathways have been elucidated, the molecular etiologies of ASD are not fully understood. Previous microarray analysis in our laboratory identified differentially expressed genes between osASD and normal right auricular myocardium. Of the 1056 differentially expressed genes, 14 genes were related to apoptosis: eight pro-apoptotic genes were up-regulated and six anti-apoptotic genes were down-regulated in ASD patients. In the current study, we utilized semi-quantitative RT-PCR, electron microscopy, TUNEL and flow cytometry to further understand the role of apoptosis in the atrium of osASD patients. RT-PCR results confirmed differential expression data from previous microarray studies. Additionally, while apoptosis was detected in the right auricular myocardium of all osASD patients, it was absent in controls. These data suggested apoptosis may play an important role in the pathogenesis of osASD or possibly occurs as a consequence of volume overload and hemodynamic changes in right atrium of osASD patients.

The effect of red wine and wine polyphenol resveratrol on endothelial function was investigated in experimental hypercholesterolemic rabbits. Endothelial function as measured by flow-mediated dilation (FMD) in the femoral artery was 19.28+/-2.81% in control animals fed a regular diet. In contrast, rabbits fed a high-cholesterol (1.5%) diet showed a reduced endothelial function, as revealed by a 25% reduction in the measured FMD. Intragastric feeding of resveratrol (3 mg/kg/day), red wine (4 ml/kg/day), dealcoholized red wine (4 ml/kg/day), for 12 weeks in hypercholesterolemic rabbits significantly mitigated the reduction in endothelial function, and resulted in FMD values of 14.52+/-0.60, 18.95+/-2.30, 17.58+/-1.43, and 18.80+/-3.94%, respectively. Measurement of plasma endothelin 1 (ET-1) and nitric oxide (NO) levels showed that feeding a high-cholesterol diet significantly increased plasma ET-1 levels (from 51.4+/-17.6 to 96.9+/-24.3 pg/ml), and decreased plasma NO concentration (from 104.6+/-18.5 to 67.7+/-16.1 pg/ml). With administration of resveratrol, red wine, or dealcoholized red wine, plasma ET-1 levels statistically decreased, in parallel with a significant elevation in NO levels. These results provide in vivo evidence suggesting that resveratrol and red wine improve endothelial function, which may be one of the mechanisms by which this red wine polyphenol exerts its alcohol-independent cardioprotective effects.

To investigate changes in the expression of sarcoplamic reticular Ca(2+)-ATPase (SERCA) and IP(3)-I receptors (IP(3)R(1)) mRNA in patients with atrial fibrillation.Thirty-eight patients with mitral stenosis undergoing open heart surgery were studied. 100 mg of atrial tissue was obtained during surgery from the right appendage and the right atrium. The amount of messenger ribonucleic acid (mRNA) amount of SERCA and IP(3)R(1) was measured by reverse transcription-polymerase chain reaction (RT-PCR) and normalized to the mRNA levels of glyceraldehyde 3-phosphate dehydrogenase (GAPDH).Levels of mRNA expression of SERCA in patients with AF, as compared with subjects in sinus rhythm, was lower and that of IP(3)R(1) was higher. The longer AF was sustained, the higher the levels of mRNA. There was no significant difference between right atrial free wall and right appendage.The expression changes of SERCA and IP3R mRNA may correlate with the initiation or maintenance of AF.

Low or moderate consumption of red wine has a greater benefit than the consumption of other beverages in the prevention of atherosclerosis and coronary heart disease and this is increasingly attributed to the polyphenol compounds in red wine, such as resveratrol. In the present study, we investigated the effect of resveratrol on platelet aggregation in vitro and in vivo.Platelet aggregation in rabbits and normal subjects was measured using Born's method.Resveratrol, at 10 - 1000 micromol/L, significantly inhibited platelet aggregation in vitro induced by collagen, thrombin, and ADP in healthy subjects. The inhibitory effect was concentration-dependent. Hypercholesterolemia induced by high-cholesterol diet enhanced ADP-induced platelet aggregation. Resveratrol 4 mg x kg(-1) x d(-1) inhibited ADP-induced platelet aggregation in vivo despite no changes in serum lipid levels.Resveratrol inhibits platelet aggregation both in vitro and in vivo. This may be one of the mechanisms by which resveratrol prevents atherosclerosis.

Low to moderate consumption of red wine reportedly has a relatively greater benefit than other alcoholic beverages in the prevention of atherosclerosis and coronary heart disease (CHD). This beneficial effect is increasingly attributed to the polyphenol resveratrol, present in red wine. In the present study, we investigated the effects of resveratrol and red wine on aggregation of platelets isolated from healthy, normotensive male volunteers and in rabbits with experimental hypercholesterolemia. Platelet aggregation rate (PAR) was measured using Born's method. The results showed that aggregation of platelets from healthy subjects induced in vitro by collagen (5 microg/ml), thrombin (0.33 units/ml), and ADP (4 microM) was significantly inhibited by 10-1000 microM resveratrol, in a concentration-dependent manner. Hypercholesterolemic rabbits showed enhanced ADP-induced platelet aggregation; the average PAR increased from 39.5+/-5.9% in normal animals to 61.0+/-7.0% in the high-cholesterol fed group (n=8, p

Coronary heart disease (CHD) has been and remains a major contributor to morbidity and mortality in developed countries. The most common form of CHD in the western world is atherosclerosis (AS), especially of the major coronary arteries. Failure to maintain an intact endothelium, as a result of episodic and/or persistent injury and perturbation of the vascular endothelium, promotes formation of fatty streaks which are considered initiation events of AS. Cellular constituents contributing to endothelial injury include endothelial cells, monocytes, platelets, and smooth muscle cells. Individuals diagnosed with AS face complex, enduring clinical complications and enormous medical costs. Simple and easily compliant prevention and treatment measures are therefore strategic considerations in the management of this vascular disease. Based on known risk factors for CHD, priorities in AS prevention should include smoking cessation, blood pressure control, and diet modification. In recent years, the possible benefits of low to moderate consumption of alcoholic beverages, particularly of red wine, in the prevention of heart disease has received increasing attention and debate in the popular media as well as in the scientific community. Such attention has been prompted by research findings supporting a relationship between red wine consumption and the French paradox. This phenomenon refers to people residing in certain parts of France where red wine is customarily consumed during meals having a low CHD mortality, despite living a lifestyle considered to have comparably high CHD risks, as those in the US and many other developed countries. Studies have reported that the cardioprotective effects of red wine are greater than those attributed solely to ethanol and other types of alcoholic beverages. The mechanism(s) underlying the greater CHD protective benefits of red wine have not been elucidated. Recently the polyphenol resveratrol (3,5,4'-trihydroxy-trans-stilbene), known to be abundantly present in red wine, compared to white wine, beer, or spirits, has been demonstrated to elicit a broad spectrum of biological responses in in vitro and in animal studies, including effects that are compatible with the cardioprotective roles proposed for red wine. These recently described effects of resveratrol will be reviewed in this article. We will first summarize published data showing an inverse association between consumption of alcoholic beverages/red wine and risk of CHD. A review of biosynthesis of resveratrol and its presence in food groups and wines will follow. Recent studies relating exposure to wine/resveratrol with reduction in myocardial damage during ischemia-reperfusion, modulation of vascular cell functions, inhibition of LDL oxidation, and suppression of platelet aggregation will be presented. The last section of this review will focus on a discussion of mechanism(s) by which resveratrol acts as a potential cardioprotective agent.

The ability of resveratrol to inhibit vascular intimal thickening was tested in an experimental model in which endothelial denudation was performed in the normal rabbit iliac artery. Resveratrol (2 approximately 4mg/ kg/d) was administered intragastrically for 5 weeks beginning 1 week before denudation. At the higher concentration of resveratrol, the intimal hyperplasia of injured vascular wall was effectively inhibited; the intimal proliferation index also was significantly less than that in the untreated control group (0.28 +/- 0.07 vs 0.41 +/- 0.13, respectively, p0.01); the relative luminal area increased from 0.38 +/- 0.06 in the untreated control group to 0.53 +/- 0.10 in the resveratrol treatment group (p0.001); and the count of smooth muscle cells in the thickened intima was statistically significantly reduced in the high dose resveratrol treatment group than that in the untreated group (1,115 +/- 510 vs 1,796 +/- 963, respectively, p0.05). Resveratrol added to the culture media of cultured rabbit vascular smooth muscle cells inhibited DNA synthesis in a dose-dependent manner. These results showing that resveratrol is capable of inhibiting intimal hyperplasia of injured artery raise the possibility that this polyphenol might have clinical potential in prevention and treatment of restenosis after angioplasty.