From prospecting to mining: A review of enabling technologies, LCAs, and LCCAs for improved construction and demolition waste management.

Knowledge gained from anthropogenic resource prospecting can shed light on the theoretical potential of secondary resources stored in anthropogenic systems. Among others, secondary resources accumulated in the built environment account for a big fraction of anthropogenic resources, indicating great potential for urban mining. However, realizing these opportunities and developing urban mining strategies will require a comprehensive understanding of the technical viability of urban mining technologies, and how their implementation will affect the technical, economic, and environmental performance of a construction and demolition waste (C&DW) management system. To address these important issues, this review summarizes (1) current and emerging technologies that can enable the transition from anthropogenic resource prospecting to anthropogenic resource mining, (2) Life Cycle Assessment (LCA) and Life Cycle Cost Analysis (LCCA) results to date on various C&DW management systems, (3) key parameters that govern the technical, economic, and environmental performance of a C&DW management system, and (4) opportunities for improving the methodology of LCAs and LCCAs for future C&DW management. We find that enhancing the utility of extant LCAs and LCCAs in guiding technology deployment and policy decisions can be achieved by considering key parameters governing the techno-economic and environmental performance of C&DW management. In addition, it is critical to adopt and upscale emerging technologies to increase the added value of materials or products recovered from C&DW.

FTO inhibits oxidative stress by mediating m6A demethylation of Nrf2 to alleviate cerebral ischemia/reperfusion injury

Current therapies are of limited efficacy in cerebral ischemia/reperfusion (I/R) injury. Based on the important role of oxidative stress in cerebral I/R injury, this study aimed to explore how the N6-adenosine methylation (m6A) demethylase FTO affects oxidative stress. Middle cerebral artery occlusion/reperfusion (MCAO/R)-induced rat model and oxygen and glucose deprivation/re-oxygenation (OGD/R)-induced SH-SY5Y cells were established as in vivo and in vitro model, respectively. The neurological score of rats was measured, and the volume of cerebral infarction was measured by TTC staining. The levels of FTO, nuclear factor-erythroid 2-related factor (Nrf2), and the activity of m6A demethylase FTO were detected. The m6A methylation level of Nrf2 mRNA was detected by MeRIP experiment. Flow cytometry and MTT assay were used to detect apoptosis and proliferation in vitro. TUNEL assay was used to detect apoptosis in brain tissues. FTO and Nrf2 expressions were decreased in the MCAO/R rat brain tissues and OGD/R SH-SY5Y cells, while the m6A methylation level of Nrf2 mRNA was significantly increased. Overexpression of FTO upregulated Nrf2 expression by decreasing the m6A methylation level of Nrf2 mRNA. m6A binding protein YT521-B homology (YTH) domain family protein 2 (YTHDF2) promoted the degradation of Nrf2 by promoting the m6A methylation level of Nrf2 mRNA. Furthermore, SH-SY5Y cell apoptosis was increased and cell viability was decreased after the addition of methyltransferases METTL 3/14, thus blocking FTO to protect SH-SY5Y cells from oxidative stress injury. In vivo, overexpression of FTO decreased the area of cerebral ischemia infarction and the extent of cell apoptosis. In conclusion, FTO increases Nrf2 expression by mediating m6A demethylation of Nrf2 mRNA, thereby inhibiting oxidative stress response and ultimately alleviating cerebral I/R injury. (AU)

FTO inhibits oxidative stress by mediating m6A demethylation of Nrf2 to alleviate cerebral ischemia/reperfusion injury.

Current therapies are of limited efficacy in cerebral ischemia/reperfusion (I/R) injury. Based on the important role of oxidative stress in cerebral I/R injury, this study aimed to explore how the N6-adenosine methylation (m6A) demethylase FTO affects oxidative stress. Middle cerebral artery occlusion/reperfusion (MCAO/R)-induced rat model and oxygen and glucose deprivation/re-oxygenation (OGD/R)-induced SH-SY5Y cells were established as in vivo and in vitro model, respectively. The neurological score of rats was measured, and the volume of cerebral infarction was measured by TTC staining. The levels of FTO, nuclear factor-erythroid 2-related factor (Nrf2), and the activity of m6A demethylase FTO were detected. The m6A methylation level of Nrf2 mRNA was detected by MeRIP experiment. Flow cytometry and MTT assay were used to detect apoptosis and proliferation in vitro. TUNEL assay was used to detect apoptosis in brain tissues. FTO and Nrf2 expressions were decreased in the MCAO/R rat brain tissues and OGD/R SH-SY5Y cells, while the m6A methylation level of Nrf2 mRNA was significantly increased. Overexpression of FTO upregulated Nrf2 expression by decreasing the m6A methylation level of Nrf2 mRNA. m6A binding protein YT521-B homology (YTH) domain family protein 2 (YTHDF2) promoted the degradation of Nrf2 by promoting the m6A methylation level of Nrf2 mRNA. Furthermore, SH-SY5Y cell apoptosis was increased and cell viability was decreased after the addition of methyltransferases METTL 3/14, thus blocking FTO to protect SH-SY5Y cells from oxidative stress injury. In vivo, overexpression of FTO decreased the area of cerebral ischemia infarction and the extent of cell apoptosis. In conclusion, FTO increases Nrf2 expression by mediating m6A demethylation of Nrf2 mRNA, thereby inhibiting oxidative stress response and ultimately alleviating cerebral I/R injury.

Antioxidant Effects of Roasted Licorice in a Zebrafish Model and Its Mechanisms.

Licorice (Gan-Cao, licorice) is a natural antioxidant and roasted licorice is the most common processing specification used in traditional Chinese medicine prescriptions. Traditional Chinese medicine theory deems that the honey-roasting process can promote the efficacy of licorice, including tonifying the spleen and augmenting "Qi" (energy). The antioxidant activity and mechanisms underlying roasted licorice have not yet been reported. In this study, we found that roasted licorice could relieve the oxidative stress injury induced by metronidazole (MTZ) and could restrain the production of excessive reactive oxygen species (ROS) induced by 2,2'-azobis (2-methylpropionamidine) dihydrochloride (AAPH) in a zebrafish model. It was further found that roasted licorice could exert its oxidative activity by upregulating the expression of key genes such as heme oxygenase 1 (HO-1), NAD(P)H quinone dehydrogenase 1 (NQO1), glutamate-cysteine ligase modifier subunit (GCLM), and glutamate-cysteine ligase catalytic subunit (GCLC) in the nuclear factor erythroid 2-related factor 2 (NRF2) signaling pathway both in vivo and in vitro. Furthermore, consistent results were obtained showing that rat serum containing roasted licorice was estimated to reduce cell apoptosis induced by H2O2. Then, the UHPLC-Q-Exactive Orbitrap MS analysis results elucidated the chemical composition of rat plasma containing roasted licorice extracts, including ten prototype chemical components and five metabolic components. Among them, six compounds were found to have binding activity with Kelch-like ECH-associated protein 1 (KEAP1), which plays a crucial role in the transcriptional activity of NRF2, using a molecular docking simulation. The results also showed that liquiritigenin had the strongest binding ability with KEAP1. Immunofluorescence further confirmed that liquiritigenin could induce the nuclear translocation of NRF2. In summary, this study provides a better understanding of the antioxidant effect and mechanisms of roasted licorice, and lays a theoretical foundation for the development of a potential antioxidant for use in clinical practice.

SLC20A2-related primary familial brain calcification with purely acute psychiatric symptoms: a case report.

BACKGROUND: Primary familial brain calcification (PFBC) is a rare inherited neurological disorder characterized by bilateral basal ganglia calcification with a series of motor and nonmotor symptoms. Mutations in the SLC20A2 gene, encoding the PiT2 protein, are the major cause of the disease. Here, we report a Chinese PFBC family carrying a SLC20A2 gene mutation, and the proband presented with purely acute psychiatric symptoms, which has been rarely reported in this disease. CASE PRESENTATION: A 38-year-old woman was hospitalized due to disorganized speech; disordered thought contents; disorganized behaviour; emotional instability and lability; and grandiose words, actions and facial expressions. Brain computerized tomography (CT) revealed calcification in the basal ganglia; cerebellar dentate nuclei; and subcortical, periventricular, and deep white matter regions in she and her family members. Through mutation analysis, a heterozygous truncating mutation, c.1723G > T, p.(Glu575*), was identified in the SLC20A2 gene in this family. Thus, this patient was diagnosed with genetically confirmed PFBC, and she responded well to a low dose of antipsychotic drugs. The penetrance of the disease in this family was only 33%, which was significantly lower than that in most families carrying SLC20A2 gene mutations. CONCLUSIONS: Patients with SLC20A2-related PFBC might present with psychiatric symptoms alone, and the penetrance of the disease may be quite low, which adds to the clinical heterogeneity of the disease.

The Mechanism of Long Non-coding RNA MEG3 for Neurons Apoptosis Caused by Hypoxia: Mediated by miR-181b-12/15-LOX Signaling Pathway.

OBJECTIVE: lncRNAs are recently thought to play a significant role in cellular homeostasis during pathological process of diseases by competing inhibiting miRNA function. The aim of present study was to assess the function of long non-coding RNA (lncRNA) MEG3 and its functional interaction with microRNA-181b in cerebral ischemic infarct of mice and hypoxia-induced neurons apoptosis. METHODS: To address this question, we performed the experiments with in vivo middle cerebral artery occlusion (MCAO) mice model and in vitro oxygen-glucose deprivation (OGD)-cultured neuronal HT22 cell line. Relative expression of MEG3, miR-181b, and 12/15-LOX (lipoxygenase) mRNA was determined using quantitative RT-PCR. Western blot was used to evaluate 12/15-LOX protein expression. TUNEL assay was performed to assess cell apoptosis. RESULTS: In both MCAO mice and OGD-cultured HT22 cell, ischemia, or hypoxia treatment results in a time-dependent increase in MEG3 and 12/15-LOX expression and decrease in miR-181b expression. Knockdown of MEG3 contributes to attenuation of hypoxia-induced apoptosis of HT22 cell. Also, expression level of MEG3 negatively correlated with miR-181b expression and positively correlated with 12/15-LOX expression. In contrary to MEG3, miR-181b overexpression attenuated hypoxia-induced HT22 cell apoptosis, as well as suppressed hypoxia-induced increase in 12/15-LOX expression. By luciferase reporter assay, we concluded that miR-181b directly binds to 12/15-LOX 3'-UTR, thereby negatively regulates 12/15-LOX expression. CONCLUSION: Our data suggested that long non-coding RNA MEG3 functions as a competing endogenous RNA for miR-181b to regulate 12/15-LOX expression in middle cerebral artery occlusion-induced ischemic infarct of brain nerve cells.

[Study on changes of content of Tannin in Nodus Nelumbinis Rhizomatis Charcoal].

OBJECTIVE: To determine changes of content of Tannin in different Nodus Nelumbinis Rhizomatis Charcoal. METHODS: The content of Tannin of Nodus Nelumbinis Rhizomatis Charcoal was detected by UV and colorimetric method. RESULTS: The content of tannin in standard sample was the highest. CONCLUSION: It should be studied whether the tannin of Nodus Nelumbinis Rhizomatis Charcoal is the active ingredients of hemostasis.

Identification and expression profile of a putative basement membrane protein gene in the midgut of Helicoverpa armigera.

BACKGROUND: The midgut undergoes histolysis and remodeling during the larval to adult transition in holometabolous insects, but the molecular mechanisms underlying this process are not well understood. RESULTS: Using Suppression Subtractive Hybridization (SSH), we identified a 531 bp cDNA predicted to encode a 176 amino acid protein, which we call hmg176. Northern and western blot analysis suggested that high levels of hmg176 are expressed in the midgut during molting, but not during metamorphosis. HMG176 protein was detected by immunofluorescence within the membrane of fat bodies and the basement membrane of the midgut of both molting and feeding larvae, but not in metamorphically committed larvae. In situ hybridization revealed that hmg176 transcripts mainly localized to the columnar cells of the midgut. Interestingly, a non-steroidal ecdysone agonist, RH-2485, significantly upregulated expression of hmg176. CONCLUSION: These observations suggest that hmg176 encodes a larval-specific protein that may participate in sustaining larval midgut during larval development, possibly in response to ecdysteroid in vivo. This study will enlighten our understanding of the molecular mechanisms of tissue histolysis during metamorphosis.

Expression and function of cathepsin B-like proteinase in larval hemocytes of Helicoverpa armigera during metamorphosis.

Previous work has revealed that Helicoverpa armigera cathepsin B-like proteinase (HCB) is expressed in oocytes as well as fat bodies of pupae and adults. It plays key roles in the degradation of yolk proteins during embryogenesis and the decomposition of adult fat bodies of H. armigera. This study investigated the expression and function of HCB in larval hemocytes during larva-pupa metamorphosis. Results showed that the expression of HCB in hemocytes exhibited developmental stage specificity. No HCB was found in hemocytes from 5th-molting larvae. On the contrary, HCB was highly transcribed in the hemocytes from 6th-48-h larvae. Besides, it was abundantly translated in 6th-96-h larvae (prepupation). HCB is mainly expressed in plasmatocytes and granulocytes at both transcriptional and translational levels. The number of plasmatocytes and granulocytes markedly increased before pupation. In addition, hemocytes distributed in hematopoietic organs at early larval stage, then migrated to midgut and fat bodies that would undergo histolysis at later larval stage. These findings suggested that HCB is expressed in H. armigera larval hemocytes and involved in larva-pupa metamorphosis.

Cathepsin B-like proteinase is involved in the decomposition of the adult fat body of Helicoverpa armigera.

Cathepsin B-like proteinase (HCB, EC 3.4.22.1) is expressed in Helicoverpa armigera oocytes and adult fat bodies. Previous work has revealed that HCB plays a key role in the degradation of yolk proteins during embryogenesis. This study investigated the function and regulatory activation of HCB in adult fat bodies during aging and oogenesis. The HCB transcript was detected at all stages from larval to adult fat bodies with Northern blot analysis. Pro-HCB was also detected in fat bodies at these stages with an immunoblot assay using a monoclonal antibody against HCB. However, mature HCB and its activity were only detected in fat bodies of pre-adults and adults. This evidence suggested that HCB is regulated post-translationally by activation of the pro-enzyme during the pupa-adult metamorphosis. The activation of HCB was coupled with the expression of hormone receptor 3 (HHR3), and was up-regulated by the ecdysteroid agonist, RH-2485, suggesting that HCB activation is related to the ecdysone regulatory system. The decomposition of the adult fat bodies during aging and oogenesis was found to occur via programmed cell death, in which HCB took part.