Abnormal expression of PRKAG2-AS1 in endothelial cells induced inflammation and apoptosis by reducing PRKAG2 expression.

PRKAG2 is required for the maintenance of cellular energy balance. PRKAG2-AS1, a long non-coding RNA (lncRNA), was found within the promoter region of PRKAG2. Despite the extensive expression of PRKAG2-AS1 in endothelial cells, the precise function and mechanism of this gene in endothelial cells have yet to be elucidated. The localization of PRKAG2-AS1 was predominantly observed in the nucleus, as revealed using nuclear and cytoplasmic fractionation and fluorescence in situ hybridization. The manipulation of PRKAG2-AS1 by knockdown and overexpression within the nucleus significantly altered PRKAG2 expression in a cis-regulatory manner. The expression of PRKAG2-AS1 and its target genes, PRKAG2b and PRKAG2d, was down-regulated in endothelial cells subjected to oxLDL and Hcy-induced injury. This finding suggests that PRKAG2-AS1 may be involved in the mechanism behind endothelial injury. The suppression of PRKAG2-AS1 specifically in the nucleus led to an upregulation of inflammatory molecules such as cytokines, adhesion molecules, and chemokines in endothelial cells. Additionally, this nuclear suppression of PRKAG2-AS1 facilitated the adherence of THP1 cells to endothelial cells. We confirmed the role of nuclear knockdown PRKAG2-AS1 in the induction of apoptosis and inhibition of cell proliferation, migration, and lumen formation through flow cytometry, TUNEL test, CCK8 assay, and cell scratching. Finally, it was determined that PRKAG2-AS1 exerts direct control over the transcription of PRKAG2 by its binding to their promoters. In conclusion, downregulation of PRKAG2-AS1 suppressed the proliferation and migration, promoted inflammation and apoptosis of endothelial cells, and thus contributed to the development of atherosclerosis resulting from endothelial cell injury.

[Health Impact Analysis of Fine Particulate Pollution from Vehicles in the Beijing-Tianjin-Hebei Region].

Vehicle exhaust emissions are posing an increasingly adverse impact on urban air quality. The emission characteristics analysis and health effect assessment of specific air pollution sources can provide scientific evidence for environmental air quality management. The characteristics and health effects of PM2.5 emissions from vehicles and economic losses caused by them in the Beijing-Tianjin-Hebei Region were analyzed from 2010 to 2020. From 2010 to 2020, PM2.5 emissions from vehicles in the Beijing-Tianjin-Hebei Region showed an annual increase at first, followed by a slow decrease. According to the emission sharing ratios of different vehicle types, heavy-duty trucks and buses were the main contributors to PM2.5, with a total contribution rate of over 65.27%. The emission characteristics of vehicle pollutants varied in different cities. The contribution rate of pollutants in Beijing decreased significantly, and the emission reduction in other cities was also dramatic. The evaluation results of the impact of PM2.5 emissions from vehicles on human health showed that the number of health endpoints in the Beijing-Tianjin-Hebei Region was on the rise. In 2020, PM2.5 pollution caused approximately 34337 premature deaths (95% CI:9025-57209), 45500 hospitalizations (95% CI:10800-80200), 282300 outpatients (95% CI:140500-416300), and 439000 people to fall ill (95% CI:160300-679200). Beijing had the largest number of patients that presented different health endpoints. The total health and economic losses caused by PM2.5 emissions from vehicles in 2010, 2015, and 2020 were 27.742 billion yuan (95% CI:8.616-44.643 billion yuan), 90.608 billion yuan (95% CI:28.476-144.050 billion yuan), and 129.965 billion yuan (95% CI:40.829-205.245 billion yuan), respectively. In addition, due to the differences in vehicle ownership, PM2.5 concentrations, population, and economic losses per case of health outcome, the health effects and economic losses varied in different cities within the region. Among these cities, Beijing, Tianjin, Baoding, and Tangshan were at higher health risks and suffered more economic losses. The results of this study will help reduce the adverse effects on health and economic losses caused by pollution discharge and provide scientific evidence for environmental protection authorities to implement targeted pollution prevention and control.

Abnormal expression of PRKAG2-AS results in dysfunction of cardiomyocytes through regulating PRKAG2 transcription by interacting with PPARG.

The role of PRKAG2 in the maintenance of heart function is well established, but little is known about how PRKAG2 is regulated in cardiomyocytes. In this study, we investigated the role of the lncRNA PRKAG2-AS, which is present at the PRKAG2 promoter, in the regulation of PRKAG2 expression. PRKAG2-AS expression was predominantly nuclear, as determined by RNA nucleoplasmic separation and fluorescence in situ hybridization. Knockdown of PRKAG2-AS in the nucleus, but not the cytoplasm, significantly decreased the expression of PRKAG2b and PRKAG2d. Interestingly, we found that PRKAG2-AS and its target genes, PRKAG2b and PRKAG2d, were reduced in the hearts of patients with ischemic cardiomyopathy, suggesting a potential role for PRKAG2-AS in myocardial ischemia. Indeed, knockdown of PRKAG2-AS in the nucleus resulted in apoptosis of cardiomyocytes. We further elucidated the mechanism by which PRKAG2-AS regulates PRKAG2 transcription by identifying 58 PRKAG2-AS interacting proteins. Among them, PPARG was selected for further investigation based on its correlation and potential interaction with PRKAG2-AS in regulating transcription. Overexpression of PPARG, or its activation with rosiglitazone, led to a significant increase in the expression of PRKAG2b and PRKAG2d in cardiomyocytes, which could be attenuated by PRKAG2-AS knockdown. This finding suggests that PRKAG2-AS mediates, at least partially, the protective effects of rosiglitazone on hypoxia-induced apoptosis. However, given the risk of rosiglitazone in heart failure, we also examined the involvement of PRKAG2-AS in this condition and found that PRKAG2-AS, as well as PRKAG2b and PRKAG2d, was elevated in hearts with dilated cardiomyopathy (DCM) and that overexpression of PRKAG2-AS led to a significant increase in PRKAG2b and PRKAG2d expression, indicating that up-regulation of PRKAG2-AS may contribute to the mechanism of heart failure by promoting transcription of PRKAG2. Consequently, proper expression of PRKAG2-AS is essential for maintaining cardiomyocyte function, and aberrant PRKAG2-AS expression induced by hypoxia or other stimuli may cause cardiac dysfunction.

Downregulation of NUP93 aggravates hypoxia-induced death of cardiomyocytes in vitro through abnormal regulation of gene transcription.

Nuclear pore complex in the nuclear envelope plays an important role in controlling the transportation of RNAs, proteins and other macromolecules between the nucleus and cytoplasm. The relationship between abnormal expression of nucleoporins and cardiovascular diseases is unclear. In this study we investigated how myocardial infarction affected the expression and function of nucleoporins in cardiomyocytes. We separately knocked down 27 nucleoporins in rat primary myocardial cells. Among 27 nucleoporins, knockdown of Nup93, Nup210 and Nup214 markedly increased the expression of ANP and BNP, two molecular markers of cardiomyocyte function. We showed that Nup93 was significantly downregulated in hypoxic cardiomyocytes. Knockdown of Nup93 aggravated hypoxia-induced injury and cell death of cardiomyocytes, whereas overexpression of Nup93 led to the opposite effects. RNA-seq and bioinformatics analysis revealed that knockdown of Nup93 did not affect the overall transportation of mRNAs from the nucleus to the cytoplasm, but regulated the transcription of a large number of mRNAs in cardiomyocytes, which are mainly involved in oxidative phosphorylation and ribosome subunits. Most of the down-regulated genes by Nup93 knockdown overlapped with the genes whose promoters could be directly bound by Nup93. Among these genes, we demonstrated that Nup93 knockdown significantly down-regulated the expression of YAP1. Overexpression of YAP1 partially rescued the function of Nup93 knockdown and attenuated the effects of hypoxia on cell injury and cardiomyocyte death. We conclude that down-regulation of Nup93, at least partially, contributes to hypoxia-induced injury and cardiomyocyte death through abnormal interaction with the genome to dynamically regulate the transcription of YAP1 and other genes. These results reveal a new mechanism of Nup93 and might provide new therapeutic targets for the treatment of ischemia-induced heart failure.

[Application of Pu isotope tracing technique in soil erosion research]. / PuåŒä½ç´ ç¤ºè¸ªæŠ€æœ¯åœ¨åœŸå£¤ä¾µèš€ç ”ç©¶ä¸­çš„åº”ç”¨.

As an essential form of material migration on the surface of the earth, soil erosion is one of the primary causes of soil fertility reduction and environmental degradation. Quantifying soil erosion rate is the precondition and foundation for regional soil erosion control. The Pu isotopes produced by atmospheric nuclear tests have a long half-life after settling into the soil and could be easily adsorbed by clay minerals and organic matter. In recent years, Pu isotopes have become principal trace elements in the quantitative studies of soil erosion rate, especially with the development of mass spectrometry technique. The measurement time of Pu isotopes has been shortened, and the sensitivity of Pu isotopes has been improved, both of which help improve the radionuclide tracing technology for soil erosion. Here, we summarized the distribution characteristics as well as the adsorption and migration behavior of Pu isotopes in soil. We described the basic principles for the application of Pu isotopes in tracing soil erosion, and elaborated the research progress concerning relevant applications. Moreover, we compared the applicability of Pu isotope and 137Cs tracing techniques in soil erosion research and proposed research directions in the future. This review would provide a reference for the scientific applications of Pu isotope tracing technique in soil erosion research.

Cardiovascular-specific PSEN1 deletion leads to abnormalities in calcium homeostasis.

Mutations of PSEN1 have been reported in dilated cardiomyopathy pedigrees. Understanding the effects and mechanisms of PSEN1 in cardiomyocytes might have important implications for treatment of heart diseases. Here, we showed that PSEN1 was downregulated in ischemia-induced failing hearts. Functionally, cardiovascular specific PSEN1 deletion led to spontaneous death of the mice due to cardiomyopathy. At the age of 11 months, the ratio of the heart weight/body weight was slightly lower in the Sm22a-PSEN1-KO mice compared with that of the WT mice. Echocardiography showed that the percentage of ejection fraction and fractional shortening was significantly reduced in the Sm22a-PSEN1-KO group compared with the percent of these measures in the WT group, indicating that PSEN1-KO resulted in heart failure. The abnormally regulated genes resulted from PSEN1-KO were detected to be enriched in muscle development and dilated cardiomyopathy. Among them, several genes encode Ca2+ ion channels, promoting us to investigate the effects of PSEN1 KO on regulation of Ca2+ in isolated adult cardiomyocytes. Consistently, in isolated adult cardiomyocytes, PSEN1-KO increased the concentration of cytosolic Ca2+ and reduced Ca2+ concentration inside the sarcoplasmic reticulum (SR) lumen at the resting stage. Additionally, SR Ca2+ was decreased in the failing hearts of WT mice, but with the lowest levels observed in the failing hearts of PSEN1 knockout mice. These results indicate that the process of Ca2+ release from SR into cytoplasm was affected by PSEN1 KO. Therefore, the abnormalities in Ca2+ homeostasis resulted from downregulation of PSEN1 in failing hearts might contribute to aging-related cardiomyopathy, which might had important implications for the treatment of aging-related heart diseases.

Light- and temperature-assisted spin state annealing: accessing the hidden multistability.

Among responsive multistable materials, spin crossover (SCO) systems are of particular interest for stabilizing multiple spin states with various stimulus inputs and physical outputs. Here, in a 2D Hofmann-type coordination polymer, [Fe(isoq)2{Au(CN)2}2] (isoq = isoquinoline), a medium-temperature annealing process is introduced after light/temperature stimulation, which accesses the hidden multistability of the spin state. With the combined effort of magnetic, crystallographic and Mössbauer spectral investigation, these distinct spin states are identified and the light- and temperature-assisted transition pathways are clarified. Such excitation-relaxation and trapping-relaxation joint mechanisms, as ingenious interplays between the kinetic and thermodynamic effects, uncover hidden possibilities for the discovery of multistable materials and the development of multistate intelligent devices.

Effects of time delays on the therapeutic outcomes of intravenous thrombolysis for acute ischemic stroke in the posterior circulation: An observational study.

OBJECTIVES: We aim to demonstrate the effects of time delays on the therapeutic outcomes of intravenous thrombolysis (IVT) in acute posterior circulation stroke (PCS) patients. METHODS: Consecutive PCS cases treated with IVT alone were retrospectively examined. The primary end point was set to be a favorable outcome (modified Rankin Scale [mRS] ≤2) at 3 months, and angiographic recanalization was set to be the secondary outcome. RESULTS: A total of 95 PCS cases with IVT were recruited. The patients with favorable outcomes and those without favorable outcomes had similar baseline characteristics, except for significantly lower National Institute of Health Stroke Scale (NIHSS) scores (5 vs. 12, respectively; p < 0.001) and less hyperdense basilar artery signs in head CTs (26.5% vs. 70.4%, respectively; p < 0.001) for those with favorable outcomes. For patients with an onset-to-treatment time (OTT) of 0-90 min (n = 5), 91-180 min (n = 38), 181-270 min (n = 37), or ≧271 min (n = 15), the rate of favorable outcome was 100.0%, 71.1%, 67.6%, or 73.3%, respectively, and the Cochran-Armitage trend test showed no linear trend between the OTT and the clinical prognosis of IVT in PCS (p = 0.501) patients. In addition, the rates of recanalization were 100.0%, 68.4%, 64.9%, and 46.7%, and the Cochran-Armitage trend test suggested a linear trend between the OTT and recanalization (p = 0.046); that is, the proportion of PCS patients who underwent recanalization decreased with increasing OTTs. In the multivariate logistic regression analysis, after adjusting for confounding factors with p â‰¦ 0.20 in the univariate analysis, baseline NIHSS scores and hyperdense basilar artery signs were negatively associated with favorable outcomes, with odds ratios (OR) of 0.884 (95% confidence interval [CI], 0.804-0.971; p = 0.010) and 0.208 (95% CI, 0.062-0.693; p = 0.011), respectively. In addition, there was a negative association between recanalization, OTTs (OR, 0.993, 95% CI, 0.987-0.999; p = 0.029), and baseline NIHSS scores (OR, 0.881, 95% CI, 0.802-0.967; p = 0.008). CONCLUSION: Irrespective of stroke severity, the therapeutic effects of recanalization after IVT decreased significantly with longer time delays in PCS patients.

Novel insight into the role of withering process in characteristic flavor formation of teas using transcriptome analysis and metabolite profiling.

Withering is an indispensable process for improving flavors in green, black and white teas during their manufacturing. The effects of the withering process on the formation of tea flavors were investigated using transcriptome and metabolite profiling in withered tea leaves. A total of 3268, 23,282 and 25,185 differentially expressed genes (DEGs) were identified at 3 h (68%, water content), 12 h (61%) and 24 h (48%) of the withering process, respectively. The DEGs, involved in flavonoid biosynthesis were significantly downregulated, which could be correlated with the reduction of catechins. Enhancement of terpenoids and alpha-linolenic acid metabolism could trigger an increase in the total content and number of volatiles. The increase in free amino acid-content could be related to 261 DEGs. Our study suggests that dehydration stress during withering induced significant changes in the gene transcription and content of the tea flavor compounds, which promoted the special flavors in various teas.

Plasma miR-451 with echocardiography serves as a diagnostic reference for pulmonary hypertension.

Due to the lack of typical clinical symptoms, the average delay time for diagnosis of pulmonary hypertension (PH) is longer than 2 years. It is urgent to find biomarkers for PH diagnosis. In this study we investigated whether plasma microRNAs (miRNAs) can be used as biomarkers for PH diagnosis. We used microarray to identify dynamic miRNAs between PH and non-PH patients. The candidate miRNAs were verified using qRT-PCR in a mouse model of PH, which was induced by monocrotaline (MCT) injection. We observed that miR-21, miR-126, miR-145, miR-191 and miR-150 had no differences between control mice and MCT-treated mice; but plasma miR-451 was significantly decreased in the 2wk-MCT group, with no further decrease in the 4wk-MCT group. Plasma miR-451 was also markedly decreased in PH patients, whereas miR-21, miR-126, miR-150 and miR-320 did not show differences between 53 PH patients and 54 non-PH patients. Receiver operating characteristic curves (ROCs) were constructed from the patient data to assess the clinical diagnostic values of circulating miR-451 and Doppler echocardiography (D-ECHO). The areas under the curve (AUCs) of ROCs for miR-451 and D-ECHO were 0.710 and 0.766, respectively. Combination of miR-451 and D-ECHO with AUC of 0.825 was superior to the use of either miR-451 or D-ECHO alone for PH diagnosis. In conclusion, plasma miR-451 has a moderate diagnostic value in PH comparable to that of D-ECHO, and the combination of miR-451 with D-ECHO has better diagnostic value than either method alone, which may have implications for PH diagnosis.

Identifying external nutrient reduction requirements and potential in the hypereutrophic Lake Taihu Basin, China.

Reducing external nutrient loads is the first step for controlling eutrophication. Here, we identified external nutrient reduction requirements and potential of strategies for achieving reductions to remediate a eutrophic water body, Lake Taihu, China. A mass balance approach based on the entire lake was used to identify nutrient reduction requirements; an empirical export coefficient approach was introduced to estimate the nutrient reduction potential of the overall program on integrated regulation of Taihu Lake Basin (hereafter referred to as the "Guideline"). Reduction requirements included external total nitrogen (TN) and total phosphorus (TP) loads, which should be reduced by 41-55 and 25-50%, respectively, to prevent nutrient accumulation in Lake Taihu and to meet the planned water quality targets. In 2010, which is the most seriously polluted calendar year during the 2008-2014 period, the nutrient reduction requirements were estimated to be 36,819 tons of N and 2442 tons of P, and the potential nutrient reduction strategies would reduce approximately 25,821 tons of N and 3024 tons of P. Since there is a net N remaining in the reduction requirements, it should be the focus and deserves more attention in identifying external nutrient reduction strategies. Moreover, abatement measures outlined in the Guideline with high P reduction potential required large monetary investments. Achieving TP reduction requirement using the cost-effective strategy costs about 80.24 million USD. The design of nutrient reduction strategies should be enacted according to regional and sectoral differences and the cost-effectiveness of abatement measures.

Conditionally targeted deletion of PSEN1 leads to diastolic heart dysfunction.

Recently, PSEN1 has been reported to have mutations in dilated cardiomyopathy pedigrees. However, the function and mechanism of PSEN1 in cardiomyopathy remains unresolved. Here, we established four types of genetically modified mice to determine the function of PSEN1 in cardiac development and pathology. PSEN1 null mutation resulted in perinatal death, retardation of heart growth, ventricular dilatation, septum defects, and valvular thickening. PSEN1 knockout in adults led to decreased muscle fibers, widened sarcomere Z lines and reduced lengths of sarcomeres in cardiomyocytes. Cardiovascular loss of function of PSEN1 induced by Sm22a-Cre or Myh6-Cre/ER/tamoxifen also resulted in severe ultrastructural abnormalities, such as relaxed gap junctions between neighboring cardiomyocytes. Functionally, cardiovascular deletion of PSEN1 caused spontaneous mortality from birth to adulthood and led to diastolic heart dysfunction, including decreased volume of the left ventricle at the end-systolic and end-diastolic stages. Additionally, in a myocardial ischemia model, deletion of PSEN1 in the cardiovascular system first protected mice by inducing adaptive hypertrophy but ultimately resulted in severe heart failure. Furthermore, a collection of genes was abnormally expressed in the hearts of cardiac-specific PSEN1 knockout mice. They were enriched in cell proliferation, calcium regulation, and so on. Taken together, dynamic regulation and abnormal function of PSEN1 underlie the pathogenesis of cardiovascular diseases due to ultrastructural abnormality of cardiomyocytes.

MicroRNA-199a acts as a potential suppressor of cardiomyocyte autophagy through targeting Hspa5.

Autophagy is an adaptive response to cardiomyocytes survival under stress conditions. MicroRNAs (miRNAs, miR) have been described to act as potent modulators of autophagy. To investigate whether and how miR-199a modulated autophagy in vitro, primary cardiomyocytes were treated under starvation to induce autophagy. Results showed that down-regulation of miR-199a was sufficient to activate cardiomyocytes autophagy. MiR-199a suppressed cardiomyocytes autophagy through direct inhibiting heat shock protein family A member 5 (Hspa5). Forced overexpression of Hspa5 recovered the inhibitory effect of miR-199a in autophagy activation. Our results suggested miR-199a as an effective suppressor of starvation-induced cardiomyocytes autophagy and that Hspa5 was a direct target during this process. These results extend the understanding of the role and pathway of miR-199a in cardiomyocytes autophagy, and may introduce a potential therapeutic strategy for the protection of cardiomyocytes in myocardial infarction or ischemic heart disease.

Out-of-Band Radiation and Spatio-Temporal Characterization of Gd Target Laser Plasma Sources.

In this paper, an Nd∶YAG laser with 10ns pulse width and output wavelength of 1 064 nm was employed to ablate Gd metal target and Gd-doped glass target for plasma generation. The out-of-band (OOB) radiation of extreme ultraviolet sources with the two target configurations was comparatively studied. It has been found that the continuous radiation emitted by the plasma is the main component of the out-of-band radiation. The spectral distribution of the continuum emission matches that of blackbody radiation with a temperature of about 5 eV. And it is also found that the intensity of OOB radiation can be considerably decreased by using Gd-doped glass target. Optical Emission Spectroscopy (OES) has been used to analyze the temporal and spatial behaviors of electron temperature (Te) and density (Ne) of the Gd-doped glass target plasma, and experimental results show that temporal evolution of electron temperature and density of the plasma are found to be decayed exponentially with the increasing of delay time. At 125 ns after laser irradiation, electron temperature and density were 4 eV and 1.2×1018 cm-3 respectively, and then decreased to 1.5 eV and 8×1017 cm-3 with delaying time of 250 ns. On the other hand, spatial evolution of electron temperature and density show that both of them first increase and then decrease in the region of 1~10 mm from the target surface. The electron temperature and electron density achieves the maximum of 2.6 eV and 8.5×1017 cm-3, respectively, when the probe location away from the target surface 6 mm.

[Analysis of arsenic speciation in food condiments based on the online trapping/separation coupling system].

An online coupling system based on gas chromatography-hydride generation with atomic fluorescence spectrometry (GC-HG-AFS) for the analysis of arsenic species in food seasoning(soy sauce and vinegar) was developed. With absorbent cotton as separation medium, the volatile arsenic species released from the samples were cold trapped online by liquid nitrogen. Then, the baseline separation of the volatile arsenic species was achieved at the room temperature and the arsenic species were sensitively detected by atomic fluorescence spectrophotometer. The experimental conditions such as flow rates of carrier .gas (He), acid type and concentration, reducing reagent concentration and reaction time were discussed. Under the optimum conditions, the limit of detection for As(III), As(V), MMA(V) and DMA(V) was 0.2, 0.2, 0.3 and 0.8 ng x mL(-1), respectively. The recoveries of As(III), As(V), MMA(V) and DMA(V) in soy sauce and vinegar were 93.07%-103.54%. Compared with the traditional liquid chromatography separation algorithm, the method was rapid, sensitive without any complex sample pretreatment. It was suitable and practical for detection of arsenic especially inorganic arsenic in food seasoning.

Prognosis in very young women with triple-negative breast cancer: retrospective study of 216 cases.

The aim of this investigation was to compare clinical pathological characteristics and prognosis of very young and older triple-negative breast cancer (TNBC) patients in order to assess their relevance to TNBC in an younger population. Data of TNBC patients diagnosed between 2002 and 2007 were retrospectively analyzed by computer based chart information. Baseline tumor characteristics, biological markers, and patients' prognosis were compared between very young (≤ 35 years) and older (>35 years) TNBC patients. In the 216 cases of operable TNBC patients, 48 (22.2%) were ≤ 35 years and 168 (77.8%) were >35 years. Very young TNBC patients had showed a high clinical stage, more positive lymph nodes, Ck5/6 and/or EGFR expression (P = 0.049, 0.006, and 0.011, respectively). Compared to older TNBC patients, very young TNBC patients have short disease-free survival (P = 0.031), while no significant difference was found in overall survival (OS) (P = 0.075). In multivariate analysis, lymph node metastatic status was a significant predictor of OS. TNBC of very young patients is an aggressive breast cancer subtype, but the overall survival of both young and older TNBC patients did not have significant differences.

Topological organization of the human brain functional connectome across the lifespan.

Human brain function undergoes complex transformations across the lifespan. We employed resting-state functional MRI and graph-theory approaches to systematically chart the lifespan trajectory of the topological organization of human whole-brain functional networks in 126 healthy individuals ranging in age from 7 to 85 years. Brain networks were constructed by computing Pearson's correlations in blood-oxygenation-level-dependent temporal fluctuations among 1024 parcellation units followed by graph-based network analyses. We observed that the human brain functional connectome exhibited highly preserved non-random modular and rich club organization over the entire age range studied. Further quantitative analyses revealed linear decreases in modularity and inverted-U shaped trajectories of local efficiency and rich club architecture. Regionally heterogeneous age effects were mainly located in several hubs (e.g., default network, dorsal attention regions). Finally, we observed inverse trajectories of long- and short-distance functional connections, indicating that the reorganization of connectivity concentrates and distributes the brain's functional networks. Our results demonstrate topological changes in the whole-brain functional connectome across nearly the entire human lifespan, providing insights into the neural substrates underlying individual variations in behavior and cognition. These results have important implications for disease connectomics because they provide a baseline for evaluating network impairments in age-related neuropsychiatric disorders.

[Removal of calcium and high-strength ammonia nitrogen from the wastewater of rare-earth elements hydrometallurgical process by chemical precipitation].

A lot of high-strength ammonia nitrogen wastewater is generated in the ion-type rare-earth elements hydrometallurgical process. Magnesium ammonium phosphate (MAP) precipitation was chosen to remove the ammonia nitrogen from the wastewater after Ca2+ was eliminated using Na2CO3 to generate CaCO3 precipitate, because the wastewater contained a lot of Ca2+, and Ca2+ was an important impact factor for MAP precipitation. Central composite design (CCD) is a principal response surface methodology (RSM) used in experimental design. Response surface methodology (RSM) was used to optimize the factors in MAP precipitation, achieving the optimal conditions and the precipitates under such conditions. Two kinds of precipitates were analyzed by scanning electron microscope (SEM) and X-ray diffraction (XRD). The results showed that when n (Ca2+): n (CO3(2-) = 1:1.05, mix rate and reaction time were 1500 r x min(-1) and 30 min, respectively, the removal ratio of Ca2+ reached 100%; the optimal condition of MAP precipitation was pH = 9.03, n (Mg): n (N) = 1.20, n (P) : n (N) = 1.1, with a reaction time of 30 min and a mix rate of 1000 r x min(-1), the removal ratio of ammonia nitrogen reached 95.40% and the residual total phosphorus concentration was 5.65 mg x L(-1). SEM and XRD analysis showed that the two kinds of precipitates were pure CaCO3 and MgNH4PO4 x 6H2O, respectively.

Dye removal of activated carbons prepared from NaOH-pretreated rice husks by low-temperature solution-processed carbonization and H3PO4 activation.

A coupling of low-temperature sulfuric acid-assisted carbonization and H3PO4 activation was employed to convert NaOH-pretreated rice husks into activated carbons with extremely high surface area (2028 m(2) g(-1)) and integrated characteristics. The influences of the activation temperature and impregnation ratio on the surface area, pore volume of activated carbons were thoroughly investigated. The morphology and surface chemistry of activated carbons were characterized using N2 sorption, FTIR, XPS, SEM, TEM, etc. The adsorption capacity of resulting carbons obtained under optimum preparation conditions was systematically evaluated using methylene blue under various simulated conditions. The adsorption process can be well described by both Langmuir isotherm model and the pseudo-second order kinetics models; and the maximum monolayer capacity of methylene blue was ca. 578 mg g(-1).