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Oxidative stress has been implicated in the pathogenesis of atherosclerotic cardiovascular diseases. Dietary supplementation of anti-oxidants has been reported to have beneficial effects on the prevention of atherogenic diseases. Luteolin (a natural flavonoid) has been shown to possess antimutagenic, antitumorigenic, anti-oxidant and anti-inflammatory properties. However, the effects and underlying molecular mechanisms of luteolin on cardiovascular systems are poorly explored. Therefore, the aim of the present study was to test whether luteolin could protect against oxidative stress-induced endothelial cell injury and explore the underlying mechanisms. In this study, human umbilical vein endothelial cells (HUVECs) were pre-treated with luteolin followed by hydrogen peroxide induction (H2O2). Our results showed that luteolin protected against H2O2-induced oxidative stress and ameliorated ROS and superoxide generation. In addition, we found that luteolin treatment inhibited the H2O2-induced membrane assembly of NADPH oxidase subunits, which was further confirmed by specifically inhibiting NADPH oxidase using DPI treatment. Furthermore, pAMPK protein expression was enhanced and p-PKC isoforms were significantly down-regulated by luteolin treatment in a dose-dependent manner, and a similar effect was observed upon DPI treatment. However, co-treatment with the specific inhibitor of AMPK (Compound C) restored p-PKC levels suggesting the role of AMPK signaling in regulating p-PKC expression under oxidative stress condition in HUVECs. Finally, we confirmed using siRNAs and specific inhibitor and/or activator of AMPK (AICAR) that luteolin treatment induced AMPK is a key player and regulator of activated expression of PKC isoforms and thereby confers protection against H2O2-induced oxidative stress in HUVECs. [ABSTRACT FROM AUTHOR]

Dilong is an earthworm extract with a dense nutritional content, widely used in Chinese herbal medicine to remove stasis and stimulate wound healing. Earthworm extracts are traditionally used by indigenous people throughout the world. How this Dilong inhibits Lipopolysaccharide (LPS)-induced cardiomyoblast cell apoptosis is still unclear. This study investigates the Dilong extract effect on LPS-induced apoptosis in H9c2 cardiomyoblast cells. LPS (1 μg/ml) administration for 24 h induced apoptosis in H9c2 cells. Cell apoptosis was detected using MTT, LDH, TUNEL assay and JC-1 staining. Western blot analysis was used to detect pro-apoptotic and anti-apoptotic proteins. Dilong extract totally blocked the LPS impact, leading to the activation of anti-apoptotic proteins, Bcl-2 and Bcl-xL, stabilized the mitochondria membrane and down-regulated the extrinsic and intrinsic pro-apoptotic proteins, TNF-α, active caspase-8, t-Bid, Bax, active caspase-9 and active caspase-3. Dilong could potentially serve as a cardio protective agent against LPS-induced H9c2 cardiomyoblast cell apoptosis. [ABSTRACT FROM AUTHOR]

As Chinese calligraphy moves into today's world, it is interestingly divorcing itself from its original nature. Calligraphy is clearly being affected by the multi-dimensional cultural of out time, which has set off many experiments in the exploration of new possibilities for this traditional art. These experimental works attempt to align themselves with contemporary art, and they essentially deviate from traditional calligraphy. Set against the long history of Chinese calligraphy, this recent development is a radical change, unique in calligraphic history. It is this author's opinion that, while it is necessary to break age-old constraints, the distinct forms and materials of calligraphy should be acknowledged and used in adapting to the new era. By examining calligraphic schools and exhibitions in China, Japan, and Taiwan in recent years, this paper intends to illuminate how the art of calligraphy is transforming itself in the present-day world. [ABSTRACT FROM AUTHOR]

Development of Alzheimer's disease (AD) is characterized by progressive neuronal death and a decline in learning and memory. Mutations in human senataxin (SETX), an ortholog yeast protein of Sen1, have been identified to cause the syndrome of ataxia with oculomotor apraxia type 2 (AOA2) and juvenile amyotrophic lateral sclerosis (ALS4), two types of progressive motor neuron degeneration. However, the relationship between the SETX gene, which is involved in the regulation of RNA processing and DNA repair, and the predisposition for AD remains unclear. In this research, potential association of polymorphisms in the SETX gene with AD was investigated. A case-control study of a Chinese Han population in Taiwan was performed. Three single-nucleotide polymorphisms (SNPs), 3455T>G (rs3739922), 3576T>G (rs1185193) and 7759A>G (rs1056899) were studied. The experimental data showed that upon genotyping of the exonic polymorphism in the SETX gene, the T allele appeared at a lower rate than the G allele at position 3455 in AD patients compared with normal groups (P < 0.05, odds ratio (OR), 0.59, 95% confidence interval (CI), 0.40-0.89). Subjects with the GA genotype at position 7759 have higher incidences of AD development than with the AA genotype (P < 0.05, OR, 6.45, 95% CI, 1.24 to 33.70). Our results also showed that with six haplotypes (Hts) observed from the analyzed polymorphisms, distributions of the Ht4-GAA and Ht5-GCA haplotypes appeared to be significant 'risk' haplotypes between AD patients and controls (both P < 0.05, OR, 8.44, 95% CI, 1.07-66.60). These observations suggest that genetic variations in the SETX gene may contribute to AD pathogenesis in the Taiwanese Han population.

Antibodies against the proliferating cell nuclear antigen (PCNA) was first discovered in the sera of systemic lupus erythematosus (SLE) patients. However, the reactivity and specificity of anti-PCNA autoantibodies are still unclear. To investigate the property of anti-PCNA autoantibodies, we conducted an ELISA screening of the anti-PCNA autoantibodies in sera of SLE patients. Eighteen out of 191 SLE sera were found to be positive for anti-PCNA antibodies giving a frequency of nearly 10%. Among the positive sera, a sample with the highest titer of anti-PCNA autoantibody preferentially recognizes the wild-type PCNA as compared to the Y114A mutation which contains a single amino acid substitution at 114 and fails to form the toroidal structure. Moreover, the autoantibody purified from this serum identifies only the free PCNA in crude mammalian cell extracts but not other associated cellular components. This finding raises a possibility that immunostaining with the human anti-PCNA autoantibodies in previous studies might have only partially PCNAs in tissues.