Enhanced OER catalytic activity of single metal atoms supported by the pentagonal NiN2 monolayer: insight from density functional theory calculations.

Two-dimensional material-supported single metal atom catalysts have been extensively studied and proved effective in electrocatalytic reactions in recent years. In this work, we systematically investigate the OER catalytic properties of single metal atoms supported by the NiN2 monolayer. Several typical transition metals with high single atom catalytic activity, such as Fe, Co, Ru, Rh, Pd, Ir, and Pt, were selected as catalytic active sites. The energy calculations show that transition metal atoms (Fe, Co, Ru, Rh, Pd, Ir, and Pt) are easily embedded in the NiN2 monolayer with Ni vacancies due to the negative binding energy. The calculated OER overpotentials of Fe, Co, Ru, Rh, Pd, Ir and Pt embedded NiN2 monolayers are 0.92 V, 0.47 V, 1.13 V, 0.66 V, 1.25 V, 0.28 V, and 0.94 V, respectively. Compared to the 0.57 V OER overpotential of typical OER noble metal catalysts IrO2, Co@NiN2 and Ir@NiN2 exhibit high OER catalytic activity due to lower overpotential, especially for Ir@NiN2. The high catalytic activity of the Ir embedded NiN2 monolayer can be explained well by the d-band center model. It is found that the adsorption strength of the embedded TM atoms with intermediates follows a linear relationship with their d-band centers. Besides, the overpotential of the Ir embedded NiN2 monolayer can be further reduced to 0.24 V under -2% biaxial strain. Such findings are expected to be employed in more two-dimensional material-supported single metal atom catalyzed reactions.

Knockdown of Long Noncoding RNAs of Maternally Expressed 3 Alleviates Hyperoxia-Induced Lung Injury via Inhibiting Thioredoxin-Interacting Protein-Mediated Pyroptosis by Binding to miR-18a.

Long-term hyperoxia exposure may cause lung damage with characteristic inflammation. Long noncoding RNA of maternally expressed 3 (MEG3) is up-regulated in lung tissues exposed to hyperoxia; however, the underlying mechanism is unclear. Hyperoxia-induced cells and mouse models were used to study these mechanisms. Molecular assays were used to detect cell viability, cytotoxicity, and expression of miR-18a, MEG3, and inflammatory cytokines. The interaction among MEG3, miR-18a, and thioredoxin-interacting protein (TXNIP) was verified; and pyroptosis-related proteins were analyzed. The in vivo model was established by exposing MEG3 knockdown mice to hyperoxia. Hematoxylin and eosin staining was used to assess pathologic alterations of lung tissues. Hyperoxia suppressed cell viability, induced cell damage, and exacerbated the secretion of IL-1ß and IL-18. Hyperoxia inhibited miR-18a, with increased expression of MEG3, TXNIP, and nonobese diabetic-like receptor family pyrin domain containing 3 (NLRP3). MEG3 aggravated TXNIP expression by binding to miR-18a. Knockdown of MEG3 rescued hyperoxia-induced pyroptosis by up-regulating miR-18a. Furthermore, knockdown of MEG3 inhibited NLRP3 inflammasome activity and caspase-1 signaling by miR-18a. In vivo knockdown of MEG3 and overexpression of miR-18a relieved hyperoxia-induced lung injury via restraining NLRP3 inflammasome-mediated pyroptosis, whereas miR-18a inhibition reversed these effects. In conclusion, knockdown of MEG3 inhibits pyroptosis to alleviate hyperoxia lung injury by suppressing NLRP3 inflammasome and caspase-1 signaling via regulating miR-18a-TXNIP axis.

Roles of the mammalian target of rapamycin (mTOR) signaling pathway in the repair of hyperoxia-induced acute lung injury.

BACKGROUND: Rapamycin inhibits the mammalian target of rapamycin (mTOR) activity and has been proven effective for the treatment of lung injury. OBJECTIVES: The objective of this study was to investigate the roles of the mTOR pathway and its inhibitor rapamycin in the repair of hyperoxia-induced acute lung injury (ALI). MATERIAL AND METHODS: Firstly, premature rat lung fibroblast L929 cells were cultured under different oxygen concentrations (40%, 60%, and 90%). At day 3, 7 and 14 after exposure, MTT assay and flow cytometry were used to evaluate the effect of oxygen stress on cell viability and apoptosis of L929 cells, respectively. Secondly, microscopy, MTT assay and flow cytometry was used to investigate the effect of 10 nM rapamycin on 90% O2 exposed L929 cells. We also used small interfering RNAs (siRNAs) to abrogate the expression of mTOR in 90% O2 exposed L929 cells, and then evaluated the apoptosis and cell viability using flow cytometry and the MTT assay, respectively. In addition, western blot was used to detect the protein expression of Bcl-2, p53, TGF-ß and connective tissue growth factor (CTGF). A hyperoxia-induced lung injury model was established in Sprague Dawley (SD) rats in order to evaluate the histopathological changes in lung tissues and expression of the mTOR pathway and fibrosis related factors. RESULTS: Exposure to 40%, 60% or 90% oxygen all significantly inhibited the growth of L929 cells. Application of 10 nM rapamycin was found to effectively promote apoptosis of 90% O2 exposed L929 cells. In addition, mTOR siRNA promoted the apoptosis and inhibited the growth of L929 cells. Rapamycin inhibited the activation of the mTOR signaling pathway, down-regulated the expression of downstream proteins p70S6K and 4EBP1, reduced the collagen deposition and the production of fibrosis-inducing factors, including TGF-ß and CTGF in hyperoxia-induced lung injury rats. CONCLUSIONS: Rapamycin may be useful for the treatment of hyperoxia-induced acute lung injury (ALI) by inhibiting the activation of mTOR signaling pathway.

Long-term use of methamphetamine disrupts the menstrual cycles and hypothalamic-pituitary-ovarian axis.

OBJECTIVES: Long-term use of methamphetamine (MA) induces the neuron damage and leads to multiple neuropsychiatric disorders. However, the effect of MA on the female reproductive functions has not yet been evaluated. The objective of this study was to determine the prevalence of abnormal menstrual cycling in female MA users. METHODS: Female MA users (N = 113) were recruited from the Zhangjiang Isolated Compulsory Detoxification Center. Gynecologic history and drug use history were recorded, and serum levels of follicle-stimulating hormone, luteinizing hormone, prolactin, estrogen, progesterone, and testosterone were measured. RESULTS: Long-term use of MA significantly altered the menstrual cycle, and 33.6% women suffered from abnormal uterine bleeding while using MA. Deregulation of sex hormones was observed in 73.3% of participants during abstinence. The most common patterns were simple anovular menstruation, which was caused mainly by a hypothalamic deregulation and pituitary suppression with or without ovarian suppression. Normal hormone levels were observed more frequently in participants abstinent for more than 10 months (39.5%) than in participants who were abstinent for less than 10 months (18.6%). However, no relationship was found between hormone deregulation and age or history of MA use. CONCLUSIONS: The present data demonstrate that long-term use of MA results in the disruption of menstrual cycles and dysfunction of hypothalamic-pituitary-gonadal axis in women.

[Repair of femoral neck fracture with vascular pedicled periosteum flap transfer in young and middle-aged].

OBJECTIVE: To estimate clinical effect of spin iliac deep vascular pedicled periosteum flap in repairing traumatic femoral neck of theca inside fracture in young and middle-aged. METHODS: From April 1993 to September 2001, 12 cases of traumatic femoral neck fracture were given diaplastic operation with fixation of 3 centre hollow pressed bolt and were conducted under os traction bed and "C" arm X-ray machine. Spin iliac deep vascular pedicled periosteum flap was stripped off, and transferred to the front of femoral neck fundus, then transplanted to the narrow inside of fracture through outer open door of articular capsule. RESULTS: All patients were followed up for 1-7 years. All fracture healed without femoral head necrosis, but mild arthritis appeared in 7 cases. CONCLUSION: Vascular pedicled periosteum flap transfer of young and middle-aged femoral neck fracture, by decompression of femoral neck and reconstruction of blood circulation, can promote the fracture healing and decrease the wound and blood circulation destroy.