Plastic food? Energy compensation of zebrafish (Danio rerio) after long-term exposure to polylactic acid biomicroplastics.

The extensive use of bio-based plastics has led to their widespread distribution in the environment. However, their long-term ecological impact on aquatic animals is not well understood. In this study, adult zebrafish (Danio rerio) were exposed to 1000 items·L-1 of either polylactic acid (PLA) or polyethylene terephthalate (PET) microplastics (MPs), for 90 days. PLA is a typical bio-based plastic, while PET is a typical petroleum-derived plastic. The abundances of PLA and PET MPs in fish intestines were 981 ± 66 and 671 ± 151 items per fish, respectively, indicating a greater amount of PLA MP residues than PET MPs. However, the inhibitory effect of PET on fish weight was 1.8 times higher than that of PLA, suggesting energy compensation in PLA-treated zebrafish. Proliferation of Lactobacillus was observed in the fish intestines of the PLA group, indicating increased utilization capacity of intestinal flora for lactic acid production during PLA degradation. Metabolomics showed that the tricarboxylic acid pathway was up-regulated in the PLA group compared with that in the PET group, providing evidence of energy compensation. However, more ingested PLA MPs caused more significant histological damage to fish intestines than PET MPs. Therefore, the ecological risks of bio-based plastics still require attention.

17ß-Estradiol inhibits hydrogen peroxide-induced senescence and apoptosis in human umbilical vein endothelial cells by regulating the THBS1/TGF-ß/Smad axis.

Before menopause, females exhibit a lower incidence of cardiovascular disease than age-matched males, possibly owing to the protective effects of sex hormones. 17ß-estradiol (17ß-E2) protects against oxidative stress-induced injury by suppressing thrombospondin-1 (THBS1) expression in endothelial cells. Here, we examined the role of 17ß-E2-mediated THBS1 suppression in preventing cell senescence and apoptosis. Human umbilical vein endothelial cells (HUVECs) were cultivated and treated with siRNA or overexpression plasmids to regulate THBS1. H2O2, estrogen-activity modulating drugs, and LY2109761 (a TGF-ß kinase inhibitor) treatments were applied. THBS1 knockdown repressed, and its overexpression aggravated, H2O2-induced cell injury, affecting cell death, proliferation, senescence, and apoptosis. 17ß-E2 inhibited THBS1 mRNA and protein expression time- and dose-dependently, by targeting ERß. THBS1 overexpression blocked 17ß-E2 from preventing H2O2-induced injury, significantly activating the TGF-ß/Smad pathway. 17ß-E2 inhibited H2O2-induced oxidative stress by downregulating THBS1 expression and TGF-ß/Smad signaling in HUVECs. The THBS1/TGF-ß/Smad axis could thus be a therapeutic target.

Association between serum omega-3 PUFAs levels and cognitive impairment in never medically treated first-episode patients with geriatric depression: A cross-sectional study.

BACKGROUND: Geriatric depression increases the public health burden and health care costs, reduces quality of life. Studies have shown the association between ω-3 PUFAs levels and inflammatory markers levels and depression, but few have explored the relationship between omega-3 PUFAs, inflammatory markers, and cognitive function in geriatric depression. This study aimed to compare the differences in ω-3 PUFAs levels and inflammatory markers between geriatric depression with cognitive impairment (CI) and those without CI. METHODS: A total of three hundred and five elderly patients were recruited. In addition to collecting basic information, their blood specimens were collected to detect serum EPA, DHA, AA, TC, LDL-C, IL-6, TNF-α, and hs-CRP levels. The Hamilton depression scale (HAMD), Hamilton anxiety scale (HAMA), and The Montreal cognitive assessment (MoCA) were used to assess their depression, anxiety, and cognitive function, respectively. RESULTS: Compared to those without CI, geriatric depression patients with CI had higher serum TC, LDL-C levels, lower EPA, DHA, and AA levels, and more elevated IL-6, TNF-α, and hs-CRP levels (all P < 0.05). Further linear regression analysis showed that EPA, DHA, and TNF-α, hs-CRP levels were significantly associated with the occurrence and the severity of CI. LIMITATIONS: No causal relationship could be drawn due to the cross-sectional design. CONCLUSIONS: Omega-3 PUFAs and inflammatory factors levels may predict CI in elderly patients with MDD in the future. Our findings suggest that ω-3 PUFAs (EPA and DHA) and inflammatory factors (TNF-α and CRP) may predict the occurrence and the severity of CI among elderly MDD patients.

The Legal Correspondence of Sexual Self-Defense Capability Assessment.

OBJECTIVES: To understand the legal application and case deposition of assessment opinions of sexual self-defense capability, and to explore the necessity of legal correspondence in the sexual defense capability assessment. METHODS: According to the self-made questionnaire, the cases of sexual self-defense capability assessment completed by the Academy of Forensic Science from January 1, 2012 to December 31, 2018 were statistically analyzed through telephone interviews and referrals. RESULTS: Among the 69 cases, 3 cases (4.3%) had complete sexual self-defense capability, 30 cases (43.5%) had weakened sexual self-defense capability, 32 cases (46.2%) had no sexual self-defense capability, and 4 cases (5.8%) were not suitable for assessment. Among the 30 cases with weakened sexual self-defense ability, 15 cases were filed and investigated by public security authorities for rape and 15 cases were not. The inconsistent rate of disposition was 1∶1. Among the 15 rape cases filed and investigated by the public security authorities, 10 cases were arrested and prosecuted by the procuratorate and sentenced to fixed-term imprisonment by the court, while the other 5 cases were not arrested and prosecuted by the procuratorate, with an inconsistent rate of disposition being 2∶1. CONCLUSIONS: The legal application of the assessment opinion on the weakening of sexual self-defense capability is inconsistent, and the judicial disposition is confusing. It is imperative to unify and correspond the classification of sexual self-defense capability with the legal requirements.

Research progress on the application of feed additives in ruminal methane emission reduction: a review.

BACKGROUND: Ruminal methane (CH4) emissions from ruminants not only pollute the environment and exacerbate the greenhouse effect, but also cause animal energy losses and low production efficiency. Consequently, it is necessary to find ways of reducing methane emissions in ruminants. Studies have reported that feed additives such as nitrogen-containing compounds, probiotics, prebiotics, and plant extracts significantly reduce ruminant methane; however, systematic reviews of such studies are lacking. The present article summarizes research over the past five years on the effects of nitrogen-containing compounds, probiotics, probiotics, and plant extracts on methane emissions in ruminants. The paper could provide theoretical support and guide future research in animal production and global warming mitigation. METHODS: This review uses the Web of Science database to search keywords related to ruminants and methane reduction in the past five years, and uses Sci-Hub, PubMed, etc. as auxiliary searchers. Read, filter, list, and summarize all the retrieved documents, and finally complete this article. RESULTS: Most of the extracts can not only significantly reduce CH4 greenhouse gas emissions, but they will not cause negative effects on animal and human health either. Therefore, this article reviews the mechanisms of CH4 production in ruminants and the application and effects of N-containing compounds, probiotics, prebiotics, and plant extracts on CH4 emission reduction in ruminants based on published studies over the past 5 years. CONCLUSION: Our review provides a theoretical basis for future research and the application of feed additives in ruminant CH4 emission reduction activities.

[Personality Change due to Brain Trauma Caused by Traffic Accidents and Its Assessment of Psychiatric Impairment].

OBJECTIVE: To explore the main performance of personality change in people with mild psychiatric impairments which due to the brain trauma caused by traffic accidents and its value in assessment of psychiatric impairment. METHODS: The condition of personality change of patients with traumatic brain injury caused by traffic accident was evaluated by the Scale of Personality Change Post-traumatic Brain Injury (SPCPTBI). Furthermore, the correlation between the personality change and the degrees of traumatic brain injury and psychiatric impairment were explored. Results In 271 samples, 239 (88.2%) with personality changes. Among these 239 samples, 178 (65.7%), 46 (17.0%), 15 (5.5%) with mild, moderate and severe personality changes, respectively. The ratio based on the extent of personality changes to the degree of brain trauma was not significant (P > 0.05), but the total score difference between the groups was significant (P < 0.05). There was no statistical significance between the medium and high severity brain trauma groups. The higher degree of personality changes, the higher rank of mental disabilities. The total score difference of the scale of personality change among the different mild psychiatric impairment group was significant (P<0.05). The difference between other psychiatric impairment levels had statistical significance (P < 0.05) except level 7 and 8. CONCLUSION: The occurrence of personality change due to traumatic brain injury caused by traffic accident was high. Correlations exist between the personality change and the degree of psychiatric impairment. Personality change due to brain trauma caused by traffic accident can be assessed effectively by means of SPCPTBI, and the correlation between the total score and the extent of traumatic brain injury can be found.

[Function disorder assessment on patients with mild psychiatric impairment due to road traffic accidents].

OBJECTIVE: To explore the methods to assess the function disorder of patients with mild psychiatric impairment due to road traffic accidents. METHODS: In contrast to that of the patient with physical impairment, the function disorder of the patient with mild psychiatric impairment was assessed by the standard assessment instruments, such as the Barthel index of ADL (BI), Functional Activities Questionnaire (FAQ), Social Disability Screening Schedule (SDSS), Activity of Daily Living Scale (ADL), Physical Self-maintenance Scale (PSMS), and Instrumental Activities of Daily Living Scale (IADL). RESULTS: Except BI, the each total score of FAQ, SDSS, ADL, PSMS, and IADL correlated well with the rank of psychiatric impairment. The difference of each total score of rating scales among different physical impairment rank was not statistically significant. At the impairment rank of level 10, the difference of each total score of FAQ and ADL was not significant between the two groups; each total score of BI, SDSS, and IADL in psychiatric impairment was higher than that of physical impairment, while the total score of PSMS in psychiatric impairment was lower than that of physical impairment. At the level 9, except PSMS, the each total score of BI, FAQ, SDSS, IADL and ADL in psychiatric impairment was higher than that of physical impairment. At the level 8, except BI and PSMS, the each total score of FAQ, SDSS, IADL and ADL in psychiatric impairment was higher than that of physical impairment. CONCLUSION: The different criteria for assessment of mild psychiatric and physical impairment may exist, and appropriate indexes for assessment between physical and psychiatric impairment need to be further elucidated.

Ser149 is another potential PKA phosphorylation target of Cdc25B in G2/M transition of fertilized mouse eggs.

It is well documented that protein kinase A (PKA) acts as a negative regulator of M phase promoting factor (MPF) by phosphorylating cell division cycle 25 homolog B (Cdc25B) in mammals. However, the molecular mechanism remains unclear. In this study, we identified PKA phosphorylation sites in vitro by LC-MS/MS analysis, including Ser(149), Ser(229), and Ser(321) of Cdc25B, and explored the role of Ser(149) in G(2)/M transition of fertilized mouse eggs. The results showed that the overexpressed Cdc25B-S149A mutant initiated efficient MPF activation by direct dephosphorylation of Cdc2-Tyr(15), resulting in triggering mitosis prior to Cdc25B-WT. Conversely, overexpression of the phosphomimic Cdc25B-S149D mutant showed no significant difference in comparison with the control groups. Furthermore, we found that Cdc25B-Ser(149) was phosphorylated at G(1) and S phases, whereas dephosphorylated at G(2) and M phases, and the phosphorylation of Cdc25B-Ser(149) was modulated by PKA in vivo. In addition, we examined endogenous and exogenous Cdc25B, which were expressed mostly in the cytoplasm at the G(1) and S phases and translocated to the nucleus at the G(2) phase. Collectively, our findings provide evidence that Ser(149) may be another potential PKA phosphorylation target of Cdc25B in G(2)/M transition of fertilized mouse eggs and Cdc25B as a direct downstream substrate of PKA in mammals, which plays important roles in the regulation of early development of mouse embryos.