152 research outputs found
Theoretical and experimental investigation of an absorption refrigeration and pre-desalination system for marine engine exhaust gas heat recovery
Absorption-refrigeration-cycle-based exhaust gas heat recovery technology is effective in improving the thermal efficiency and fuel economy of marine diesel engines. However, the absorption refrigeration system is inflexible in the start–stop operation, and this cannot fulfil the fluctuating demand of refrigeration. This paper presents both the theoretical and experimental investigations of an absorption refrigeration and freezing pre-desalination-based marine engine exhaust gas heat recovery system. The energy storage subcycle is introduced to overcome the energy underutilisation and balance the excessive refrigerating output of the absorption refrigeration cycle. Seawater is utilised as the phase-change material and it is pre-desalinated in the energy storage subcycle. A mathematical model of the system is established and experimental investigation is conducted. Furthermore, the theoretical and experimental performances are compared, and an economic analysis of seawater desalination is performed to evaluate its economy. The results show that the total refrigeration output of the system ranges from 6.1 kW to 9.9 kW, and the system COP (Coefficient of Performance) can reach 16% under the experimental operating conditions. Additionally, the salinity of pre-desalinated seawater can be reduced to below 10 ppt. Moreover, the cost of RO (Reverse Osmosis) seawater desalination can be reduced by 26% through the pre-desalination process of seawater
Association between type 2 inflammatory diseases and neurodevelopmental disorders in low-birth-weight children and adolescents
BackgroundEvidence of the association of certain neurodevelopmental disorder with specific type 2 inflammatory (T2) disease has been found. However, the association of various neurodevelopmental disorders with T2 diseases as a whole remains unclear in low-birth-weight (LBW) infants.ObjectiveTo evaluate the association of type 2 inflammatory (T2) diseases with intellectual disability (ID), autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), and learning disability (LD) in LBW children and adolescents.MethodsThe study sample was derived from 2005 to 2018 National Health Interview Survey sample child files. LBW children and adolescents aged 3–17 were included. History of T2 diseases (including asthma and atopic dermatitis) and four neurodevelopmental disorders were reported by adults in families. The relationship between T2 diseases and the risk of four neurodevelopmental disorders was investigated through multiple-weighted logistic regression. Age, sex, race/ethnicity, region, highest education in family and ratio of family income to the poverty threshold were adjusted as covariates for model estimation. Subgroup analyses were conducted by age stratification (3–11 and 12–17 years), sex (male and female), and race (white and non-white).Results11,260 LBW children aged 3–17 years [mean age (SE), 9.73 (0.05) years] were included, in which 3,191 children had T2 diseases. History of T2 diseases was associated with an increased risk of neurodevelopmental disorders, with an OR of 1.35 (95% CI, 0.99–1.84) for ID, 1.47 (95% CI, 1.05–2.05) for ASD, 1.81 (95% CI, 1.51–2.16) for ADHD, and 1.74 (95% CI, 1.49–2.04) for LD following the adjustment of all the covariates. The correlations between T2 disorders and each of the four neurodevelopmental disorders were significantly different by sex and race (all P for interaction < 0.001), and no differences were found in age stratification (all P for interaction > 0.05).ConclusionIn a nationally representative sample of children, we found a significant association of T2 diseases with ASD, ADHD, and LD, even after adjusting for demographic baseline. We also found that the association of T2 disease with neurodevelopmental disorders differed between sex and race. Further investigation is needed to evaluate causal relationships and elucidate their potential mechanisms
Low-degree melt metasomatic origin of heavy Fe isotope enrichment in the MORB mantle
Studies of mid-ocean ridge basalts (MORB) show a variable Fe isotope composition of the oceanic upper mantle. To test a recent hypothesis that heavy Fe isotope enrichment in the MORB mantle results from the same process of incompatible element enrichment, we conduct an Fe isotope study of well-characterized MORB samples from a magmatically robust segment (OH-1) of the Mid-Atlantic Ridge (MAR) at ∼ 35°N. The data show large Fe isotope variation (Fe = +0.03 to +0.18‰) that correlates well with the abundances and ratios of more-to-less incompatible elements and with Sr-Nd-Hf isotopes. Our findings in support of the hypothesis can be detailed as follows: (1) the oceanic upper mantle has a heterogeneous Fe isotope composition on varying small spatial scales with isotopically heavy Fe (high-Fe) preferentially associated with pyroxenite lithologies; (2) such lithologies, which are also enriched in the progressively more incompatible elements, are of low-degree (low-F) melt metasomatic origin; (3) with all the conceivable processes considered, the low-F melt metasomatism takes place at the lithosphere-asthenosphere boundary (LAB) beneath ocean basins through crystallization of incipient (Low-F) melt in the seismic low velocity zone (LVZ) at the base of the growing oceanic lithosphere (i.e., LAB) over the Earth's history since the onset of plate tectonics, forming composite lithologies with geochemically enriched pyroxenite veins dispersed in the depleted peridotite matrix; (4) such mantle of composite lithology when transported to beneath the present-day ocean ridges will undergo decompression melting and produce MORB melts with geochemical trends of “melting-induced mixing” as observed at the MAR and global MORB; (5) we predict all this to be a globally common process and widespread
Endothelium-derived Hyperpolarizing Factor (EDHF) Mediates Endothelium-dependent Vasodilator Effects of Aqueous Extracts from Eucommia ulmoides Oliv. Leaves in Rat Mesenteric Resistance Arteries
The vascular effects of an aqueous extract prepared from the leaves of Eucommia ulmoides Oliv. (ELE), a medicinal herb commonly used in antihypertensive herbal prescriptions in China, were investigated
in rat mesenteric resistance arteries. The mesenteric vascular bed was perfused with Krebs solution and the perfusion pressure was measured with a pressure transducer. In preparations with an intact endothelium and precontracted with 7μM methoxamine, perfusion of ELE (10-7-10-2mg/ml for 15min) caused a concentration-dependent vasodilatation, which was abolished by chemical removal of the endothelium. The ELE-induced vasodilatation was inhibited by neither indomethacin (INDO, a cyclooxygenase inhibitor) nor NG-nitro-L-arginine-methyl ester (L-NAME, a nitric oxide inhibitor). The ELE-induced vasodilatation was significantly inhibited by tetraethylammonium (TEA, a K+ channel blocker) and 18α-glycyrrhetinic acid (18α-GA, a gap-junction inhibitor), and abolished by high K+ -containing Krebsʼ solution. Atropine (a muscarinic acetylcholine receptor antagonist) significantly inhibited the vasodilatation induced by ELE at high concentrations. These results suggest that the ELE-induced vasodilatation is endothelium-dependent but nitric oxide (NO)- and prostaglandin I2 (PGI2)-independent, and is mainly mediated by the endothelium-derived hyperpolarizing factor (EDHF) in the mesenteric resistance arteries. Furthermore, the ELE-induced EDHF-mediated response involves the activation of K+-channels and gap junctions.</p
Lithosphere thinning beneath west North China Craton: Evidence from geochemical and Sr-Nd-Hf isotope compositions of Jining basalts
This study shows lithosphere evolution history in the west North China Craton (NCC) from the early Cretaceous to Quaternary by studying the major element, trace element and Sr-Nd-Hf isotope compositions in Jining basalts of 119.6-108.6. Ma, 23.5-21.9. Ma and 1.3-0.11. Ma.The early Cretaceous basalts (119.6-108.6Ma) display enriched characteristics with high contents of incompatible elements, high 87Sr/86Sri, low εNd(t) and low εHf(t). These basalts resulted from partial melting of ancient metasomatized lithospheric mantle, and we consider the 119.6-108.6Ma magmatism as indicating lithosphere thinning in the west NCC. Although the Pacific slab seen seismically in the mantle transition zone beneath eastern China is no older than 60Ma, there exists convincing evidence for the presence of the Paleo-Pacific slab in the transition-zone in the Mesozoic. Thus we propose that the water released from the transition-zone slab hydrated the overlying lithosphere and further converted the base of the lithosphere into asthenosphere. This is the most likely mechanism responsible for the lithosphere thinning in the west NCC and the petrogenesis of the Jining 119.6-108.6Ma basalts.The Jining 23.5-21.9Ma basalts also have high contents of incompatible elements, but they display high εNd(t), high εHf(t) and variably low 87Sr/86Sri. We propose that these Miocene basalts were derived from the asthenosphere with contributions from ancient metasomatized lithospheric mantle during melt ascent. The Jining Quaternary basalts (1.3-0.11Ma) represent the melt of upwelling asthenosphere with low 87Sr/86Sri, high εNd(t) and high εHf(t). Upwelling and decompression melting of the eastward flowing asthenosphere from beneath western plateaus to beneath eastern hilly plains in the Cenozoic is the most plausible mechanism for the petrogenesis of Jining Cenozoic basalts (both of 23.5-21.9Ma and 1.3-0.11Ma), but the Jining 1.3-0.11Ma basalts must have been produced beneath even thinner lithosphere.Taken together geophysical studies and our petrological and geochemical studies of all these three episodes of the Jining basalts, we propose that the lithosphere in the west NCC has been thinning since the early Cretaceous and the thinning continues to the present
Targeting P-Glycoprotein: Nelfinavir Reverses Adriamycin Resistance in K562/ADR Cells
Background/Aims: The emergence of multidrug resistance (MDR) caused by P-glycoprotein (P-gp) overexpression is a serious obstacle to the treatment of chronic myelocytic leukemia. In recent years, some clinical trials have shown that nelfinavir (NFV), a traditional anti-HIV drug, has anti-cancer effects. Some researchers have also shown NFV might be a potential P-gp inhibitor. This study is aimed at investigating whether nelfinavir can act as an MDR-reversal drug and to clarify its molecular mechanism as well. Methods: K562 and K562/ADR cell lines were applied in the study. Cytotoxicity was detected by CCK-8 reagents. Cell apoptosis was detected by flow cytometry and inverted fluorescence microscopy to detect the binding of apoptotic dyes to cells. Western blot was used to detect the expression of proteins. Drug-protein molecular docking simulation by using Sybyl-x 2.0 software. Results: Non-toxic concentrations of NFV (1.25–5 μM) could reverse Adriamycin (ADR), colchicine, paclitaxel, and imatinib resistance of K562/ADR cells, with reversal indexes of up to 10.8, 7.4, 57, and 9.3, respectively. NFV inhibited P-gp efflux function, as evidenced by the significant increase in the intracellular accumulation of ADR and Rho-123, without affecting P-gp protein and mRNA expression levels. Further ATP content detection and molecular docking simulations showed that NFV could decrease intracellular ATP content and has a high affinity with the active functional regions of P-gp, respectively. When co-administered with ADR, NFV increased intracellular reactive oxygen species as well as blocked the ERK/Akt signaling pathway, leading to cell apoptosis. Conclusion: NFV inhibited P-gp function, decreased intracellular ATP content, and promoted cell apoptosis in K562/ADR cells, thereby reversing MDR. These findings encourage further animal and clinical MDR studies with a combination therapy consisting of NFV and chemotherapeutic drugs
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