Effect of synthesis temperature on the structural morphology of a metal-organic framework and the capacitor performance of derived cobalt-nickel layered double hydroxides.

Three-dimensional interconnected nickel-cobalt layered double hydroxides (NiCo-LDHs) were prepared on nickel foam by ion exchange using a cobalt-based metal-organic framework (Co-MOF) as a template at different temperatures. The effects of the Co-MOF preparation temperature on the growth, mass, morphology, and electrochemical properties of the Co-MOF and derived NiCo-LDH samples were studied. The synthesis temperature from 30 to 50 °C gradually increased the mass of the active material and the thickness of the Co-MOF sheets grown on the nickel foam. The higher the temperature is, the larger the proportion of Co3+. ß-Cobalt hydroxide (ß-Co(OH)2) sheets were generated above 60 °C. The morphology and mass loading pattern of the derived flocculent layer clusters of NiCo-LDH were inherited from metal-organic frameworks (MOFs). The areal capacitance of NiCo-LDH shows an inverted U-shaped curve trend with increasing temperature. The electrode material synthesized at 50 °C had a tremendous specific capacitance of 7631 mF·cm-2 at a current density of 2 mA·cm-2. The asymmetric supercapacitor assembled with the sample and active carbon (AC) achieved an energy density of 55.0 Wh·kg-1 at a power density of 800.0 W·kg-1, demonstrating the great potential of the NiCo-LDH material for energy storage. This work presents a new strategy for designing and fabricating advanced green supercapacitor materials with large power and energy densities.

Morphologic Analysis of Congenital Heart Disease With Anomalous Tracheobronchial Arborization.

BACKGROUND: This study investigated the morphologic characteristics of congenital heart disease (CHD) combined with anomalous tracheobronchial arborization (ATBA) to provide new considerations for surgically treating congenital tracheal stenosis. METHODS: A retrospective review of surgical experience with ATBA was conducted of 147 patients. The proportion of patients with ATBA combined with tracheal stenosis was determined. Four ATBA types were identified: type A, tracheal bronchus (n = 58); type B, bronchial trifurcation (n = 46); type C, bridging bronchus (n = 38); and type D, tracheal bronchus combined with bronchial trifurcation (n = 5). The rate of tracheoplasty for each type was determined. We measured the carina/pseudocarina angle and assessed the distribution of CHD, especially pulmonary artery sling. RESULTS: The tracheal diameter of 14 patients (24.1%) with type A and 5 patients (10.9%) with type B was normal. There were 128 patients with tracheal stenosis and complete tracheal rings; of them, 113 patients received tracheoplasty. The tracheoplasty rate was higher for type C than type A (100% vs 62.1%, P < .001). The carina/pseudocarina angle was significantly reduced postoperatively (P < .001). The repair in 78 patients (60.9%) was combined with a pulmonary artery sling. A pulmonary azygos lobe was found in 10 patients (6.8%) and was resected. CONCLUSIONS: ATBA is common in patients with congenital tracheal stenosis and may be associated with abnormal embryonic development. The new classification of ATBA has clinical significance in treating patients with congenital tracheal stenosis. The poor tracheal development cannot be explained merely with vascular compression. Tracheoplasty is currently the optimal option for every type.

Risk factors for low cardiac output syndrome in children with congenital heart disease undergoing cardiac surgery: a retrospective cohort study.

BACKGROUND: Low cardiac output syndrome (LCOS) is an important complication of cardiac surgery. It is associated with increased morbidity and mortality. The incidence of LCOS after surgery is high in patients with congenital heart disease (CHD). Therefore, determining the risk factors of LCOS has clinical significance for the management of CHD. This study aimed to analyze the risk factors of LCOS. METHODS: We conducted a retrospective analysis of children with CHD who underwent cardiac surgery at Shanghai Children's Medical Center between January 1, 2014, and December 31, 2017. Demographic characteristics and baseline data were extracted from the health data resource center of the hospital, which integrates clinical routine data including medical records, diagnoses, orders, surgeries, laboratory tests, imaging, nursing, and other subsystems. Logistic regressions were performed to analyze the risk factors of LCOS. RESULTS: Overall, 8660 infants with CHD were included, and 864 (9.98%) had LCOS after surgery. The multivariate regression analysis identified that age (OR 0.992, 95% CI: 0.988-0.997, p = 0.001), tricuspid regurgitation (1.192, 1.072-1.326, p = 0.001), Risk Adjustment in Congenital Heart Surgery-1 risk grade (1.166, 1.011-1.345, p = 0.035), aortic shunt (left-to-right: 1.37, 1.005-1.867, p = 0.046; bi-directional: 1.716, 1.138-2.587, p = 0.01), atrial shunt (left-to-right: 1.407, 1.097-1.805, p = 0.007; right-to-left: 3.168, 1.944-5.163, p < 0.001; bi-directional: 1.87, 1.389-2.519, p < 0.001), ventricular level shunt (left-to-right: 0.676, 0.486-0.94, p = 0.02; bi-directional: 2.09, 1.611-2.712, p < 0.001), residual shunt (3.489, 1.502-8.105, p = 0.004), left ventricular outflow tract obstruction (3.934, 1.673-9.254, p = 0.002), right ventricular outflow tract obstruction (3.638, 1.225-10.798, p = 0.02), circulating temperature (mild hypothermia: 1.526, 95% CI: 1.205-1.934, p < 0.001; middle and low temperature: 1.738, 1.236-2.443, p = 0.001), duration of cardiopulmonary bypass (1.009, 1.006-1.012, p < 0.001), myocardial preservation using histidine-tryptophan-ketoglutarate (1.677, 1.298-2.167, p < 0.001), and mitral insufficiency (1.714, 1.239-2.37, p < 0.001) were independent risk predictors of LCOS. CONCLUSIONS: The incidence of postoperative LCOS in CHD children remains high. Circulation temperature, myocardial preservation using histidine-tryptophan-ketoglutarate, and usage of residual shunt after surgery were independent risk predictors for LCOS.

Nuclear RNF2 inhibits interferon function by promoting K33-linked STAT1 disassociation from DNA.

Prolonged activation of interferon-STAT1 signaling is closely related to inflammatory autoimmune disorders, and therefore the identification of negative regulators of these pathways is important. Through high-content screening of 115 mouse RING-domain E3 ligases, we identified the E3 ubiquitin ligase RNF2 as a potent inhibitor of interferon-dependent antiviral responses. RNF2 deficiency substantially enhanced interferon-stimulated gene (ISG) expression and antiviral responses. Mechanistically, nuclear RNF2 directly bound to STAT1 after interferon stimulation and increased K33-linked polyubiquitination of the DNA-binding domain of STAT1 at position K379, in addition to promoting the disassociation of STAT1/STAT2 from DNA and consequently suppressing ISG transcription. Our study provides insight into the regulation of interferon-dependent responses via a previously unrecognized post-translational modification of STAT1 in the nucleus.

Downregulated expression of miR-142-3p in macrophages contributes to increased IL-6 levels in aged mice.

Macrophages are innate immune cells that are important contributors to age-related functional impairment of the immune system. During the cell aging process, microRNAs are differentially expressed and participate in the regulation of aging-related immune responses. However, the role of aging-associated changes in miRNA expression in macrophages remains unclear. Here, we found that miR-142-3p expression is downregulated 50% in peritoneal macrophages from aged mice compared with young mice and is not upregulated by cell treatment with lipopolysaccharide (LPS), CpG, or polyinosinic-polycytidylic acid. Serum levels of miR-142-3p are also lower in aged mice than in young mice by q-PCR. Luciferase reporter analysis showed that IL-6 is a target of miR-142-3p in macrophages. In addition, the histone deacetylase inhibitor trichostatin A increased miR-142-3p expression by more than 3-fold in LPS-treated macrophages from aged mice compared with young mice, which in turn suppressed LPS-stimulated IL-6 production, suggesting that inhibition of miR-142-3p by histone deacetylation may be involved in the lack of response to LPS stimulation in macrophages of aged mice. These findings suggest that downregulation of miR-142-3p in macrophages of aged mice might contribute to IL-6-associated aging disorders and that epigenetic modification might be involved in age-related inflammatory diseases.