The different dissipation behavior of chiral pesticide paclobutrazol in the brine during Chinese cabbage pickling process

Paclobutrazol (PBZ) is a kind of chiral pesticide, which is a plant growth regulator and has fungicidal activity. Because of the steric‐hindrance effect, there are two enantiomers (2S, 3S; 2R, 3R) in the production. This research studied on the dissipation behavior of chiral pesticide PBZ in the brine during the Chinese cabbage pickled process by phase column‐high performance liquid chromatography (HPLC). The result demonstrated the PBZ enantiomers had the different dissipation in the brine. The study on the behavior of chiral pesticide PBZ in food may provide more sufficient data and information for understanding the potential risk in food and evaluating the environmental pollution at the enantiomer level.     

Enantioselective liquid‐liquid extraction of 3‐chloro‐phenylglycine enantiomers using (S,S)‐DIOP as extractant

(S,S)‐DIOP, a common catalyst used in asymmetric reaction, was adopted as chiral extractant to separate 3‐chloro‐phenylglycine enantiomers in liquid‐liquid extraction. The factors affecting extraction efficiency were studied, including metal precursors, organic solvents, extraction temperature, chiral extractant concentration, and pH of aqueous phase. (S,S)‐DIOP‐Pd exhibited good ability to recognize 3‐chloro‐phenylglycine enantiomers, and the operational enantioselectivity (α) is 1.836. The highest performance factor (pf) was obtained under the condition of extraction temperature of 9.1°C, (S,S)‐DIOP‐Pd concentration of 1.7 mmol/L, and pH of aqueous phase of 7.0. In addition, the possible recognition mechanism of (S,S)‐DIOP‐Pd towards 3‐chloro‐phenylglycine enantiomers was discussed.     

Retracted: Advanced glycation end-products induce oxidative stress through the Sirt1/Nrf2 axis by interacting with the receptor of AGEs under diabetic conditions

Despite the administration of exogenous insulin and other medications used to control many aspects of diabetes mellitus (DM), increased oxidative stress has been increasingly acknowledged in DM development and complications. Therefore, this study aims to investigate the role of advanced glycation end-products (AGEs) in oxidative stress (OS) of thyroid cells in patients with DM. Patients with DM with or without thyroid dysfunction (TD) were enrolled. Thyroid toxic damage was induced by adding AGE-modified bovine serum albumin (AGE-BSA) to normal human thyroid follicular epithelial cells. The cell viability, cell cycle, and cell apoptosis, as well as the content of reactive oxygen species (ROS), catalase (CAT), and malondialdehyde (MDA) in cells were measured. Thyroid hormones, T3, T4, FT3, and FT4 levels were measured by enzyme-linked immunosorbent assay. Receptor for advanced glycation end products (RAGE), sirtuin1 ( Sirt1), and NF-E2-related factor 2 ( Nrf2) expressions were detected, and the mitochondrial membrane potential was measured. We found increased AGEs in the serum of DM patients with TD. By increasing AGE-BSA concentration, cell viability; the thyroid hormones T3, T4, FT3, and FT4 levels; and mitochondrial membrane potential all significantly decreased. However, the increase in AGE-BSA concentration led to an increase in cell apoptosis, RAGE, and nuclear factor-κB expressions but produced the opposite effect on Sirt1, Nrf2, and heme oxygenase-1 expressions, as well as a decrease in antioxidant response element protein levels. The AGE-BSA increased ROS and MDA levels and reduced CAT level in normal human thyroid follicular epithelial cells on a dose independence basis. Our results demonstrated that AGEs-mediated direct increase of RAGE produced OS in thyroid cells of DM by inactivating the Sirt1/Nrf2 axis.     

Shared KEGG pathways of icariin-targeted genes and osteoarthritis

The beneficial effects of icariin in the management of many diseases, such as chronic renal failure and heart failure, are well known. Icariin has also been shown to ameliorate osteoarthritis (OA) symptoms; however, the underlying mechanisms remain unclear. In this study, a bioinformatics analysis was performed to investigate the KEGG pathways of icariin-targeted genes involved in OA. Our study suggests that icariin plays a role in OA by regulating inflammatory cytokine production, insulin resistance, and cell survival through modulation of the NF-κB, MAPK, and Akt signaling pathways. Importantly, IKBKB, NFKBIA, MAPK8, MAPK9, and MAPK10 may be the hub genes affected by icariin when providing its beneficial effects on OA. In addition, we found that icariin decreases proinflammatory factors and inhibits chondrocyte apoptosis through suppression of the NF-κB pathway. Our study highlights a set of KEGG pathways that could explain the molecular mechanism of icariin's action on OA, suggesting that icariin could be considered as a promising therapeutic option for OA.     

Association of Per3 length polymorphism with susceptibility of Alzheimer disease (AD) in Chinese population

Objectives: The association of Per3 length polymorphism with susceptibility of Alzheimer Disease (AD) was examined in the present study. Methods: This study was constructed using the case-control method and investigated the association of Per3 length polymorphism with susceptibility of AD. Genotypes of APOE and Per3 length were determined by a PCR restriction fragment length polymorphism detection method. Results: In this study, we gathered 130 unrelated AD patients and 188 controls in performing an analysis the association of Per3 length polymorphism with susceptibility of AD. In the whole sample or APOE ε4 non-carriers, an increased prevalence of five repeat homozygotes of Per3 length in AD patients had significant higher than that in controls (in the whole sample: χ² = 7.261,= 0.0176; in APOE ε4 non-carriers: χ² = 6.086, p = 0.030). And, among APOE ε4 carriers, an increased prevalence of five repeat homozygotes of Per3 length in AD patients had also significant higher than that in controls (χ² = 3.893, p = 0.0319). Conclusions: Among APOE ε4 non-carriers, five repeat homozygotes of Per3 length was associated with a high susceptibility of AD among APOE ε4 carriers and non-carriers.     

Duplex-Repair enables highly accurate sequencing,despite DNA damage

Accurate DNA sequencing is crucial in biomedicine. Underlying the most accurate methods is the assumption that a mutation is true if altered bases are present on both strands of the DNA duplex. We now show that this assumption can be wrong. We establish that current methods to prepare DNA for sequencing, via ‘End Repair/dA-Tailing,’ may substantially resynthesize strands, leading amplifiable lesions or alterations on one strand to become indiscernible from true mutations on both strands. Indeed, we discovered that 7–17% and 32–57% of interior ‘duplex base pairs’ from cell-free DNA and formalin-fixed tumor biopsies, respectively, could be resynthesized in vitro and potentially introduce false mutations. To address this, we present Duplex-Repair, and show that it limits interior duplex base pair resynthesis by 8- to 464-fold, rescues the impact of induced DNA damage, and affords up to 8.9-fold more accurate duplex sequencing. Our study uncovers a major Achilles’ heel in sequencing and offers a solution to restore high accuracy.