The Physiological Mechanism of Improved Formaldehyde Resistance in Petunia hybrida Harboring a Mammalian cyp2e1 Gene

AbstractCytochrome P450 CYP2E1 is mainly present in hepatocytes in the livers of mammals, where it plays an important role in the metabolism of xenobiotic organic substances. Previous studies showed that transgenic petunia (Petunia hybrid) plants harboring a mammalian cyp2e1 gene (designated cyp2e1-transgenic petunia) exhibited increased resistance to formaldehyde stress. In this study, we used cyp2e1-transgenic petunia plants to analyze physiological indexes related to formaldehyde stress responses. The results indicated that under formaldehyde stress, the malondialdehyde content in cyp2e1-transgenic petunia plants was lower than in β-glucuronidase gene (gus)-transgenic and wild-type petunia plants. The activities of both superoxide dismutase and peroxidase in the cyp2e1-transgenic plants were higher than in gus-transgenic and wild-type plants. The alcohol dehydrogenase activity was slightly increased and more glutathione was consumed. Additionally, under formaldehyde stress, the levels of plant hormones including indole-3-acetic acid, zeatin and abscisic acid in cyp2e1-transgenic petunia plants displayed decreasing trends, whereas the level of gibberellic acid displayed an increasing trend. In contrast, the indole-3-acetic acid, zeatin and abscisic acid levels in gus-transgenic and wild-type petunia plants displayed increasing trends, whereas the gibberellic acid level displayed a decreasing trend. At 72h after incubation of 0.5g of cyp2e1-transgenic petunia plants in 40mL of treatment solution containing formaldehyde at 50mg · L−1, the formaldehyde content remaining in the treatment solution was close to zero while approximately half of original formaldehyde remained in the treatment solutions containing gus-transgenic and wild-type petunia plants

Characterization and cytotoxicity of PAHs in PM2.5 emitted from residential solid fuel burning in the Guanzhong Plain, China

The emission factors (EFs) of polycyclic aromatic hydrocarbons (PAHs) in PM2.5 were measured from commonly used stoves and fuels in the rural Guanzhong Plain, China. The toxicity of the PM2.5 also was measured using in vitro cellular tests. EFs of PAHs varied from 0.18 mg kg(-1) (maize straw charcoal burning in a clean stove) to 83.3 mg kg(-1) (maize straw burning in Heated Kang). The two largest influencing factors on PAH EFs were air supply and volatile matter proportion in fuel. Improvements in these two factors could decrease not only EFs of PAHs but also the proportion of 3-ring to 5-ring PAHs. Exposure to PM2.5 extracts caused a concentration-dependent decline in cell viability but an increase in reactive oxygen species (ROS), tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6). PM2.5 emitted from maize burning in Heated Kang showed the highest cytotoxicity, and EFs of ROS and inflammatory factors were the highest as well. In comparison, maize straw charcoal burning in a clean stove showed the lowest cytotoxicity, which indicated a clean stove and fuel treatment were both efficient methods for reducing cytotoxicity of primary PM2.5. The production of these bioreactive factors were highly correlated with 3-ring and 4-ring PAHs. Specifically, pyrene, anthracene and benzo(a)anthracene had the highest correlations with ROS production (R = 0.85, 0.81 and 0.80, respectively). This study shows that all tested stoves emitted PM2.5 that was cytotoxic to human cells; thus, there may be no safe levels of exposure to PM2,5 emissions from cooking and heating stoves using solid fuels. The study may also provide a new approach for evaluating the cytotoxicity of primary emitted PM2.5 from solid fuel burning as well as other PM2.5 sources. (C) 2018 Elsevier Ltd. All rights reserved

GW29-e1129 Clinical Outcomes Associated with Medical Management versus Coronary Intervention in Patients with Acute Coronary Syndrome

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Rapid kidney function decline and increased risk of heart failure in patients with type 2 diabetes: findings from the ACCORD cohort : Rapid kidney function decline and heart failure in T2D.

BACKGROUND Impaired kidney function and albuminuria are associated with increased risk of heart failure (HF) in patients with type 2 diabetes (T2D). We investigated whether rapid kidney function decline over time is an additional determinant of increased HF risk in patients with T2D, independent of baseline kidney function, albuminuria, and other HF predictors. METHODS Included in the study were 7,539 participants in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) study with baseline urinary albumin-to-creatinine ratio (UACR) data, who had completed 4 years of follow-up and had ≥ 3 eGFR measurements during that period (median eGFR/year = 1.9, IQR 1.7-3.2). The association between rapid kidney function decline (eGFR loss ≥ 5 ml/min/1.73 m2/year) and odds of HF hospitalization or HF death during the first 4 years of follow-up was estimated by logistic regression. The improvement in risk discrimination provided by adding rapid kidney function decline to other HF risk factors was evaluated as the increment in the area under the Receiving Operating Characteristics curve (ROC AUC) and integrated discrimination improvement (IDI). RESULTS Over 4 years of follow-up, 1,573 participants (20.9%) experienced rapid kidney function decline and 255 (3.4%) experienced a HF event. Rapid kidney function decline was associated with a ~ 3.2-fold increase in HF odds (3.23, 95% CI, 2.51-4.16, p < 0.0001), independent of baseline CVD history. This estimate was not attenuated by adjustment for potential confounders, including eGFR and UACR at baseline as well as at censoring (3.74; 95% CI 2.63-5.31). Adding rapid kidney function decline during follow-up to other clinical predictors (WATCH-DM score, eGFR, and UACR at study entry and end of follow-up) improved HF risk classification (ROC AUC = + 0.02, p = 0.027; relative IDI = + 38%, p < 0.0001). CONCLUSIONS In patients with T2D, rapid kidney function decline is associated with a marked increase in HF risk, independent of starting kidney function and/or albuminuria. These findings highlight the importance of serial eGFR measurements over time to improve HF risk estimation in T2D

The AXH Domain of Ataxin-1 Mediates Neurodegeneration through Its Interaction with Gfi-1/Senseless Proteins

SummarySpinocerebellar ataxia type 1 (SCA1) is a neurodegenerative disease caused by an expanded glutamine tract in human Ataxin-1 (hAtx-1). The expansion stabilizes hAtx-1, leading to its accumulation. To understand how stabilized hAtx-1 induces selective neuronal degeneration, we studied Drosophila Atx-1 (dAtx-1), which has a conserved AXH domain but lacks a polyglutamine tract. Overexpression of hAtx-1 in fruit flies produces phenotypes similar to those of dAtx-1 but different from the polyglutamine peptide alone. We show that the Drosophila and mammalian transcription factors Senseless/Gfi-1 interact with Atx-1’s AXH domain. In flies, overexpression of Atx-1 inhibits sensory-organ development by decreasing Senseless protein. Similarly, overexpression of wild-type and glutamine-expanded hAtx-1 reduces Gfi-1 levels in Purkinje cells. Deletion of the AXH domain abolishes the effects of glutamine-expanded hAtx-1 on Senseless/Gfi-1. Interestingly, loss of Gfi-1 mimics SCA1 phenotypes in Purkinje cells. These results indicate that the Atx-1/Gfi-1 interaction contributes to the selective Purkinje cell degeneration in SCA1

Fungal diversity and mycotoxin contamination in dried fish products in Zhanjiang market, China

Dried fish are important dietary protein and income sources in Zhanjiang, China. Mycotoxins produced by pathogenic fungi that contaminate fish during processing can cause considerable hazard to consumer health. This study reports fungal diversity, total fungal counts and mycotoxin contamination of dried fish sold at the seafood market in Zhanjiang. Seven dried fish products (Hemibarbus maculatus, Pseudosciaena crocea, Lutjanus erythopterus, Thunnus thynnus, Scomberomorus niphonius, Eleutheronema tetradactylum, Trichiurus lepturus, n = 10) from seven retailers were analyzed for contaminated fungal species, occurrence frequency and residues analysis of four mycotoxins. Using potato dextrose agar (PDA) plate purification, morphology observation, internal transcribed spacer (ITS) sequence analysis, 25 fungal strains representing 12 genera from dried fish were systematically isolated and identified. Three dominant genera in dried fish were Fusarium sp. (80.4%), Penicillium sp. (70.7%) and Aspergillus sp.(63.9%). Other fungal genera were Neoscytalidium sp.(38.1%), Cutaneotrichosporon sp. (38.1%), Trichoderma sp.(20.3%), Naganishia sp.(15.3%), Kodamaea sp. (10.8%), Phialemoniopsis sp.(9.2%), Nigrospora sp.(7.3%), Ceriporia sp.(6.3%), Phellinus sp.(4.5%). Aspergillus flavus contamination was the higher and ranged from 1.10 × 10³ to 2.40 × 10⁴ cfu/g. The mean fungal contamination of other fungal species in dried fish ranged from 1.07 × 10² to 4.58 × 104 cfu/g. The total fungal counts of Fusarium sp. ranged from 1.09 × 10² to 2.11 × 10⁴ cfu/g, but the occurrence frequency is relatively high. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) analyses showed that mycotoxin residues were present in 12 out of the 25 dried fish tested. Aflatoxin B1 (AFB₁) was the most frequently detected and the concentration ranged from 0.03 to 3.52 μg/kg. T-2 toxin (T-2), ochratoxin A (OTA), and deoxynivalenol (DON) concentrations ranged from 0.21 to 1.53, 0.03–2.21 and 0.71 μg/kg respectively. High occurrence of fungal populations and mycotoxins in dried fish sold in the Zhanjiang market pose a potential threat to consumer health. It is recommended that in future, advanced processing methods and controlled storage condition need to be used to minimize and if possible eliminate fungal contamination during dried fish processing