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I would argue that Richard Milette’s object has been influenced by Greek elements to reconstruct its conception. He selected a classic Greek image as his vessel’s decoration. As Liopold L. Foulem describes, “the Greek prototype chosen by Milette for this series is a true-to-life hydra, a generic, stereotypical form used because of its perverse association with art museums and, more accurately, with the study of Greek painting… by using faux Greek, pseudo-restored pots and by substituting the painted narrative of the originals with a well-known contemporary easel painting”. His ceramic vase’s shape is the same with the ancient Greek vase, but it is built of many fragments, and it has obvious seam lines. Milette intends to highlight the damaged pieces, and his works are keenly collected. I believe his works are fine examples of postmodern ceramics (not sure if I got your meaning right here), because even though his image is a completely Greek scene, it cannot be described as a Greek narrative.

Background Tetramethylpyrazine (TMP) has been reported to play a significant role in the cardiovascular and neuronal diseases. But, the functions of TMP in osteoarthritis (OA) remain unclear. In this investigation, we intended to probe the protective effectiveness of TMP in lipopolysaccharide (LPS)-caused damage in ATDC5 cells. Methods ATDC5 cells were managed with LPS (5 μg/mL) for 12 h, and then the effects of TMP on these cells were evaluated. Cell viability and apoptosis of these treated cells were detected by CCK-8 and flow cytometry methods. The secretions of IL-1β, IL-6 and TNF-α were examined via applying ELISA kits. qRT-PCR was utilized to measure cell inflammatory factors and MyD88 expression. After transfection with pc-MyD88, the above-involved cell processes were reassessed, and NF-κB and p38MAPK pathways were examined by western blot assay. Results LPS treatment induced a series of inflammatory destructions, which reduced viability, accelerated apoptosis and cell inflammatory factors release in ATDC5 cells. However, TMP precondition clearly mitigated LPS-triggered ATDC5 cell injury. Additionally, TMP down-regulated MyD88 expression in LPS-treated ATDC5 cells, as well as overexpression of MyD88 overturned the impacts of TMP on LPS-induced cell injury in ATDC5 cells. Beyond that, TMP restrained LPS-triggered the activations of NF-κB and p38MAPK via repression of MyD88. Conclusion The above consequences exhibited that TMP exhibited a protective effect to lighten LPS-caused cell damage via mediating MyD88/NF-κB/p38MAPK pathways. These findings suggested that TMP perhaps an effective agent for the clinical treatment of OA.

Aminoacyl-tRNA synthetases (ARSs) are responsible for cellular protein synthesis and cell viability involving in various process of tumorigenesis. We hypothesized that genetic variants in core ARSs genes may play an important role in the development of breast cancer. Thus, we conducted a case–control study including 1064 breast cancer cases and 1073 cancer-free controls to evaluate the associations of 28 potentially functional polymorphisms in 12 core ARSs genes (AARS, CARS, EPRS, HARS, KARS, LARS, MARS, QARS, RARS, VARS, WARS, and YARS) with breast cancer risk. We found significant associations with the risk of breast cancer for rs34087264 in AARS [odds ratio (OR) = 1.15, 95% confidence interval (CI) = 1.01–1.31], rs801186 in HARS (OR = 1.29, 95% CI = 1.08–1.54), rs193466 in RARS (OR = 1.17, 95% CI = 1.02–1.35), and rs2273802 in WARS (OR = 1.14, 95% CI = 1.01–1.30). We further observed significant interactions between rs2273802 and age at the first live birth (P = 0.041), and between rs801186 and age on breast cancer risk (P = 0.018). Combined analysis of these four SNPs showed a significant allele-dosage association between the number of risk alleles and breast cancer risk (Ptrend = 2.00 × 10−4). Compared with individuals with “0–2” risk alleles, those carrying “3,” “4,” or “5 or more” risk alleles had a 1.32 (95% CI = 1.07–1.64), 1.48 (95% CI = 1.45–1.91), or 1.60 folds (95% CI = 1.06–2.41) risk of breast cancer, respectively. These findings indicate that genetic variants in core ARSs genes may modify the individual susceptibility to breast cancer in Chinese population. © 2014 Wiley Periodicals, Inc.

Three new β -dihydroagarofuran sesquiterpene polyesters, 1 β -acetoxy-8 α ,9 β -dibenzoyloxy-13-nicotinoyloxy- β -dihydroagarofuran ( 1 ), 1 β ,2 β -diacetoxy-9 α -benzoyloxy-13-nicotinoyloxy- β -dihydroagarofuran ( 2 ), and 6 α ,8 α ,9 β ,13-tetraacetoxy-1 β -cinnamoyloxy-2 β ,4 α -dihydroxy- β -dihydroagarofuran ( 3 ) were isolated from the fruits of Celastrus orbiculatus Thunb. Their structures were determined by means of extensive spectroscopic analyses (IR, ESIMS, HRESIMS, 1D and 2D NMR).

Genetic variants may influence miRNA-mRNA interaction through modulate binding affinity, creating or destroying miRNA-binding sites. Twenty-four single nucleotide polymorphisms (SNPs) that were predicted to affect the binding affinity of breast cancer-related miRNAs to 3'-untranslated regions (UTR) of known genes were genotyped in 878 breast cancer cases and 900 controls in Chinese women. Three promising SNPs (rs10494836, rs10857748 and rs7963551) were further validated in additional 914 breast cancer cases and 967 controls. The variant allele (C) of rs7963551 at 3'-UTR of RAD52 showed a consistently reduced breast cancer risk in two stages with a combined odds ratio (OR) of 0.84 [95% confidence interval (CI) = 0.75-0.95], which was more prominent among women with early age at first live birth (OR = 0.71, 95% CI = 0.58-0.87). A significant interaction was observed between rs7963551 and age at first live birth on breast cancer risk (P for interaction = 0.04). Luciferase activity assay showed a higher expression level for rs7963551 C allele as compared with A allele (P = 5.19 × 10(-3) for MCF-7 cell lines), which might be due to a reduced inhibition from a weakened binding capacity of miRNA to 3'-UTR of RAD52 harboring C allele. These findings indicate that rs7963551 located at hsa-let-7 binding site may alter expression of RAD52 through modulating miRNA-mRNA interaction and contribute to the development of breast cancer in Chinese women.

Two new neo -clerodane diterpenes, (12 S )-6 α -acetoxy-4 α ,18-epoxy-12-hydroxy-19-tigloyloxy- neo -clerod-13-en-15,16-olide ( 1 ) and 6 α ,18-diacetoxy-4 α -hydroxy-19-tigloyloxy- neo -clerod-13-en-15,16-olide ( 2 ), along with three known analogs ( 3 – 5 ) have been isolated from the whole plants of Ajuga ciliata Bunge. Their structures were elucidated on the basis of spectroscopic data analyses (IR, ESI-MS, HR-ESI-MS, HMQC, HMBC, COSY, and NOESY). The inhibitory activities on LPS-induced NO production of these diterpenes were evaluated and compounds 1 and 5 showed inhibitory effects.

Genetic variants in human microRNA (miRNA) genes may alter mature miRNA processing and/or target selection, and likely contribute to cancer susceptibility and disease progression. Previous studies have suggested that miR-101 may play important roles in the development of cancer by regulating key tumor-associated genes. However, the role of single nucleotide polymorphisms (SNPs) of miR-101 in breast cancer susceptibility remains unclear. In this study, we genotyped 11 SNPs of the miR-101 genes (including miR-101-1 and miR-101-2) in a case-control study of 1064 breast cancer cases and 1073 cancer-free controls. The results revealed that rs462480 and rs1053872 in the flank regions of pre-miR-101-2 were significantly associated with increased risk of breast cancer (rs462480 AC/CC vs AA: adjusted OR = 1.182, 95% CI: 1.030-1.357, P = 0.017; rs1053872 CG/GG vs CC: adjusted OR = 1.179, 95% CI: 1.040-1.337, P = 0.010). However, the remaining 9 SNPs were not significantly associated with risk of breast cancer. Additionally, combined analysis of the two high-risk SNPs revealed that subjects carrying the variant genotypes of rs462480 and rs1053872 had increased risk of breast cancer in a dose-response manner (P(trend) = 0.002). Compared with individuals with "0-1" risk allele, those carrying "2-4" risk alleles had 1.29-fold risk of breast cancer. In conclusion, these findings suggested that the SNPs rs462480 and rs1053872 residing in miR-101-2 gene may have a solid impact on genetic susceptibility to breast cancer, which may improve our understanding of the potential contribution of miRNA SNPs to cancer pathogenesis.

Esophageal cancer and gastric cancer have shared risk factors and inherited susceptibility. Recent genome-wide association studies have identified multiple genetic loci associated with gastric cancer risk, which may also involve in the development of esophageal cancer. Herein, we evaluated the relationship of gastric cancer risk-related variants at 1q22, 3q13.3, 5p13.1, and 8q24 with the risk of esophageal squamous cell carcinoma (ESCC) in a Chinese population with a case–control study (2139 cases and 2273 controls). We found that the T allele of rs2294008, an intronic variant of the PSCA gene at 8q24 that was previously associated with an increased risk of gastric cancer, was inversely associated with a decreased risk of ESCC (odds ratio = 0.90; 95% confidence interval, 0.81–0.99; P = 0.034). Of interest, the association of rs2294008 with ESCC was consistent with that observed in esophageal adenocarcinoma and ESCC in Caucasian populations. However, no significant associations were observed for the other three variants at 1q22 (rs4072037), 3q13.31 (rs9841504), and 5p13.1 (rs13361707). Our findings suggest that the susceptibility locus of PSCA at 8q24 may be a double-edged sword, as modulator between the carcinogenesis processes of stomach and esophagus.

Aminoacyl-tRNA synthetases (ARSs) are responsible for cellular protein synthesis and cell viability involving in various process of tumorigenesis. We hypothesized that genetic variants in core ARSs genes may play an important role in the development of breast cancer. Thus, we conducted a case-control study including 1064 breast cancer cases and 1073 cancer-free controls to evaluate the associations of 28 potentially functional polymorphisms in 12 core ARSs genes (AARS, CARS, EPRS, HARS, KARS, LARS, MARS, QARS, RARS, VARS, WARS, and YARS) with breast cancer risk. We found significant associations with the risk of breast cancer for rs34087264 in AARS [odds ratio (OR) = 1.15, 95% confidence interval (CI) = 1.01-1.31], rs801186 in HARS (OR = 1.29, 95% CI = 1.08-1.54), rs193466 in RARS (OR = 1.17, 95% CI = 1.02-1.35), and rs2273802 in WARS (OR = 1.14, 95% CI = 1.01-1.30). We further observed significant interactions between rs2273802 and age at the first live birth (P = 0.041), and between rs801186 and age on breast cancer risk (P = 0.018). Combined analysis of these four SNPs showed a significant allele-dosage association between the number of risk alleles and breast cancer risk (Ptrend = 2.00 × 10(-4) ). Compared with individuals with "0-2" risk alleles, those carrying "3," "4," or "5 or more" risk alleles had a 1.32 (95% CI = 1.07-1.64), 1.48 (95% CI = 1.45-1.91), or 1.60 folds (95% CI = 1.06-2.41) risk of breast cancer, respectively. These findings indicate that genetic variants in core ARSs genes may modify the individual susceptibility to breast cancer in Chinese population.

Chronic hepatitis B virus (HBV) infection is a challenging global health problem. To identify genetic loci involved in chronic HBV infection, we designed a three-phase genome-wide association study in Han Chinese populations. The discovery phase included 951 HBV carriers (cases) and 937 individuals who had naturally cleared HBV infection (controls) and was followed by independent replications with a total of 2,248 cases and 3,051 controls and additional replications with 1,982 HBV carriers and 2,622 controls from the general population. We identified two new loci associated with chronic HBV infection: rs3130542 at 6p21.33 (near HLA-C, odds ratio (OR) = 1.33, P = 9.49 × 10(-14)) and rs4821116 at 22q11.21 (in UBE2L3, OR = 0.82, P = 1.71 × 10(-12)). Additionally, we replicated the previously identified associations of HLA-DP and HLA-DQ variants at 6p21.32 with chronic HBV infection. These findings highlight the importance of HLA-C and UBE2L3 in the clearance of HBV infection in addition to HLA-DP and HLA-DQ.

Autophagy is a cellular process directed at recycling of cellular proteins and removal of intracellular microorganisms, which is important for balancing sources of energy at critical times in development and in response to nutrient stress. It has been reported to be a critical process in cancer initiation and progression. We hypothesized that genetic variants in critical genes of autophagy may be involve in the development of breast cancer. Thus, we systematically screened 14 potentially functional polymorphisms in six autophagy-related genes (ATG3, ATG5, ATG7, ATG10, and ATG12 and LC3) that are core components in autophagosome formation. We conducted a case-control study including 1064 breast cancer cases and 1073 cancer-free controls to evaluate the associations of these variants with breast cancer risk. We found that rs1864182 and rs10514231 in ATG10 were significantly associated with a decreased risk of breast cancer [odds ratios (OR)=0.77, 95% confidence interval (CI): 0.61-0.96, P=0.023; and OR=0.75, 95% CI: 0.59-0.93, P=0.010, respectively]. Similar protective effects for both loci were observed between subgroups stratified by ages at diagnosis/recruitment, menarche and first live birth, and status of menopause, estrogen receptor (ER) and progesterone receptor (PR). These results suggest that genetic variants in ATG10 may implicate with breast cancer susceptibility in Chinese population. Further large and functional studies are needed to confirm our findings.

BACKGROUND: A recent genome-wide association study (GWAS) has identified three new breast cancer susceptibility loci at 12p11, 12q24 and 21q21 in populations of European descent. However, because of the genetic heterogeneity, it is largely unknown for the role of these loci in the breast cancer susceptibility in the populations of non-European descent. METHODOLOGY/PRINCIPAL FINDINGS: Here, we genotyped three variants (rs10771399 at 12p11, rs1292011 at 12q24 and rs2823093 at 21q21) in an independent case-control study with a total of 1792 breast cancer cases and 1867 cancer-free controls in a Chinese population. We found that rs10771399 and rs1292011 were significantly associated with risk of breast cancer with per-allele odds ratios (ORs) of 0.85 (95% confidence interval (CI): 0.76-0.96; P = 0.010) and 0.84 (95% CI: 0.76-0.95; P = 4.50×10(-3)), respectively, which was consistent with those reported in populations of European descent. Similar effects were observed between ER/PR positive and negative breast cancer for both loci. However, we did not found significant association between rs2823093 and breast cancer risk (OR = 0.97, 95%CI = 0.76-1.24; P = 0.795). CONCLUSIONS/SIGNIFICANCE: Our results indicate that genetic variants at 12p11 and 12q24 may also play an important role in breast cancer development in Chinese women.

A recently published genome-wide association study (GWAS) in European populations identified several loci at 4q21, 4q23 and 12q24 that were associated with risk of upper aerodigestive tract (UADT) cancers, including esophageal squamous cell carcinoma (ESCC). In the current study, we conducted a case-control study in a Chinese population including 2,139 ESCC cases and 2,273 controls to evaluate the associations of six reported single nucleotide polymorphisms (SNPs) (rs1494961, rs1229984, rs1789924, rs971074, rs671 and rs4767364) with risk of ESCC. We found significant association with risk of ESCC for four SNPs, including rs1494961 in HEL308 at 4q21 [odds ratio (OR) = 1.15, 95 % confidence interval (CI) = 1.05-1.26], rs1229984 in ADH1B at 4q23 (OR = 1.24, 95 % CI = 1.13-1.36) and rs1789924 near ADH1C at 4q23 (OR = 1.20, 95 % CI = 1.03-1.39), and rs671 in ALDH2 at 12q24 (OR = 0.83, 95 % CI = 0.75-0.91). Combined analysis of these four SNPs showed a significant allele-dosage effect on ESCC risk for individuals with different number of risk alleles (P trend = 2.23 × 10(-11)). Compared with individuals with "0-2" risk allele, those carrying "3", "4" or "5 or more" risk alleles had 1.42-, 1.66-, or 1.76-fold risk of ESCC, respectively. Thus, our findings indicate that rs1494961 at 4q21, rs1229984 and rs1789924 at 4q23, and rs671 at 12q24 may be used as genetic biomarkers for ESCC susceptibility in Chinese population.

A new lathyrane diterpene (1), an unreported spectroscopic data lathyrane diterpenene (2), and two known analaogues (3 and 4) have been isolated from Euphorbia prolifera. Their structures were elucidated as (12E,2S,3S,4R,5R,6S,9S,11S,15R)-3-butyryloxy-5,15-diacetoxy-6,17-epoxylathyra- 12-en-14-one (1), (12E,2S,3S,4R,5R,6S,9S,11S,15R)-3-propionyloxy-5,15-diacetoxy-6,17- epoxylathyra-12-en-14-one (2), (12E,2S,3S,4R,5R,6S,9S,11S,15R)-3-benzoyloxy-5,15-diacetoxy -6,17-epoxylathyra-12-en-14-one (3), and 15-O-acetyl-17-hydroxyjolkinol (4) by spectroscopic methods (IR, ESIMS, HR-ESIMS, NMR, and X-ray crystallography). The inhibitory activities on LPS-induced NO production of these diterpenes were evaluated and compounds 1, 3 and 4 showed inhibitory effects.