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BackgroundTrichloroethylene (TCE) is used extensively as an industrial solvent and has been recognized as one of the major environmental pollutants. To date, > 200 cases of TCE-induced hypersensitivity dermatitis among exposed workers have been reported worldwide, and TCE exposure has become one of the critical occupational health issues in Asia.ObjectivesThe study aimed to identify genetic susceptible biomarkers associated with the TCE-induced hypersensitivity dermatitis in genes located in the human leukocyte antigen (HLA) region.MethodsFrom 1998 to 2006, 121 cases with TCE-induced hypersensitivity dermatitis and 142 tolerant controls were recruited into the population-based case–control study. We determined HLA alleles B, DRB1, DQA1, and DQB1, by sequence-based typing. p-Values were corrected for comparisons of multiple HLA alleles. In addition, we compared and analyzed the structure character of amino acid residues of HLA molecules found in participants.ResultsWe obtained complete genotyping data of 113 cases and 142 controls. The allele HLA-B*1301 was present in 83 (73.5%) of 113 patients compared with 13 (9.2%) of 142 tolerant workers (odds ratio = 27.5; 95% confidence interval, 13.5–55.7; corrected p = 1.48 × 10−21). In addition, the HLA-B*44 alleles were present in 6.2% (7/113) of patients, but were absent in TCE-tolerant workers. Residue 95 shared by HLA-B*1301 and HLA-B*44 molecules formed a different pocket F than other residues.ConclusionsThe allele HLA-B*1301 is strongly associated with TCE-induced hypersensitivity dermatitis among exposed workers and might be used as a biomarker to predict high risk individuals to TCE.

Here, a facile wet-chemistry route for the selective growth of crystalline copper (Cu) along the sides of gold nanorods (Au NRs) in the presence of a hexadecylamine (HDA) is reported. The resulting heterostructures feature part etching of copper by galvanic replacement reaction and form crystalline AuCu alloy metal on one side of the Au NRs. By virtue of the dipeptide (cysteine-phenylalanine, Cys-Phe) ligand used during synthesis, the AuCuAu heteronanorods (HNRs) exhibit strong circular dichroism (CD) in the wavelength range of 400-1000 nm. The plasmonic chirality can be tailored by increasing the length of the Au NRs, the scale of Cu nanocrystals on the Au NRs, and the amount of gold chloride for postgrowth, resulting in an anisotropy factor (g factor) as high as 0.57 × 10 −2 . The strong CD signals are attributed to the local electromagnetic field. Under circular polarized light (CPL) illumination, the chiral plasmonic AuCuAu nanostructure exhibits high efficiency for light polarization dependent reactive oxygen species ( 1 O 2 ) that is 22.31 times that of Au NRs. The results of this study demonstrate that the chiral enantiomer provides a chirality dependent avenue for highly efficient phototherapy.

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Background and AimsCholesterol over-intake is involved in the onset of nonalcoholic steatohepatitis (NASH), and hepatocellular bile acid (BA) accumulation correlates with liver injuries. However, how dietary cholesterol influences cholesterol and BA kinetics in NASH liver remains ambiguous and needs to be clarified.MethodsMolecular markers involved in cholesterol and BA kinetics were investigated at protein and mRNA levels in an already-established stroke-prone spontaneously hypertensive 5/Dmcr rat model with fibrotic steatohepatitis, by feeding a high fat-cholesterol (HFC) diet.ResultsUnlike the control diet, the HFC diet deposited cholesterol greatly in rat livers, where 3-hydroxy-3-methylglutaryl CoA reductase, low-density lipoprotein (LDL) receptor and LDL receptor-related protein-1 were expectedly downregulated, especially at 8 and 14 weeks, suggesting that cholesterol synthesis and uptake in response to cholesterol accumulation may not be disorganized. The HFC diet did not upregulate liver X receptor-α, conversely, it enhanced classic BA synthesis by upregulating cholesterol 7α-hydroxylase but downregulating sterol 12α-hydroxylase, and influenced alternative synthesis by downregulating sterol 27-hydroxylase but upregulating oxysterol 7α-hydroxylase, mainly at 8 and 14 weeks, indicating that there were different productions of primary BA species. Unexpectedly, no feedback inhibition of BA synthesis by farnesoid X receptor occurred. Additionally, the HFC diet impaired BA detoxification by UDP-glucuronosyltransferase and sulfotransferase 2A1, and decreased excretion by bile salt export pump at 8 and 14 weeks, although it induced compensatory export by multidrug resistance-associated protein-3. The disturbed BA detoxification may correlate with suppressed pregnane X receptor and constitutive androstane receptor.ConclusionsThe HFC diet may accumulate BA in rat livers, which influences fibrotic steatohepatitis progression.Electronic supplementary materialThe online version of this article (doi:10.1007/s10620-013-2747-1) contains supplementary material, which is available to authorized users.

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