Serum procalcitonin as a marker of neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD).

BACKGROUND: Neonatal Intrahepatic Cholestasis (NICCD), as the early-age stage of Citrin deficiency involving liver dysfunction, lacks efficient diagnostic markers. Procalcitonin (PCT) has been identified as a biomarker for infection as well as various organ damage. This study aimed to explore the potential of PCT as a biomarker for NICCD. METHODS: In a single-center retrospective case-control study. Serum PCT concentrations before and after treatment of 120 NICCD patients, as the study group, were compared to the same number of cholestatic hepatitis patients, as the control group. The potential value of PCT to discriminate NICCD from control disease was further explored using Receiver Operating Characteristic (ROC) curve analysis and compared to those of other inflammatory markers. RESULTS: There was a significantly higher level of PCT in NICCD patients than in the control group. PCT concentrations were only weakly correlated with neutrophil counts and CRP levels (p ˂ 0.05). At a cut-off value of 0.495 ng/mL, PCT exhibited a significantly higher diagnostic value compared to other inflammatory markers for discriminating NICCD from the control, with a sensitivity of 90.8 % and specificity of 98.3 %. CONCLUSION: PCT might be used as an initial biomarker to discriminate children with NICCD from another hepatitis disease.

CircTLK1 modulates sepsis-induced cardiomyocyte apoptosis via enhancing PARP1/HMGB1 axis-mediated mitochondrial DNA damage by sponging miR-17-5p.

INTRODUCTION: Septic cardiomyopathy is a common complication of sepsis with high morbidity and mortality, but lacks specific therapy. This study aimed to reveal the role of circTLK1 and its potential mechanisms in septic cardiomyopathy. MATERIALS AND METHODS: The in vitro and in vivo models of septic cardiomyopathy were established. Cell viability and apoptosis were detected by CCK8, TUNEL and flow cytometry, respectively. LDH, CK, SOD, MDA, ATP, 8-OHdG, NAD+/NADH ratio, ROS level, mitochondrial membrane potential and cytochrome C distribution were evaluated using commercial kits. qRT-PCR and western blotting were performed to detect RNA and protein levels. Mitochondrial DNA (mtDNA) copy number and transcription were assessed by quantitative PCR. Dual-luciferase assay, RNA immunoprecipitation and co-immunoprecipitation were performed to verify the interaction between circTLK1/PARP1 and miR-17-5p. RESULTS: CircTLK1, PARP1 and HMGB1 were up-regulated in the in vitro and in vivo models of septic cardiomyopathy. CircTLK1 inhibition restrained LPS-induced up-regulation of PARP1 and HMGB1. Moreover, circTLK1 knockdown repressed sepsis-induced mtDNA oxidative damage, mitochondrial dysfunction and consequent cardiomyocyte apoptosis by inhibiting PARP1/HMGB1 axis in vitro and in vivo. In addition, circTLK1 enhanced PARP1 expression via sponging miR-17-5p. Inhibition of miR-17-5p abolished the protective effects of circTLK1 silencing on oxidative mtDNA damage and cardiomyocyte apoptosis. CONCLUSION: CircTLK1 sponged miR-17-5p to aggravate mtDNA oxidative damage, mitochondrial dysfunction and cardiomyocyte apoptosis via activating PARP1/HMGB1 axis during sepsis, indicating that circTLK1 may be a putative therapeutic target for septic cardiomyopathy.

Transgenic Arabidopsis thaliana plants expressing a ß-1,3-glucanase from sweet sorghum (Sorghum bicolor†L.) show reduced callose deposition and increased tolerance to aluminium toxicity.

Seventy-one cultivars of sweet sorghum (Sorghum bicolor L.) were screened for aluminium (Al) tolerance by measuring relative root growth (RRG). Two contrasting cultivars, ROMA (Al tolerant) and POTCHETSTRM (Al sensitive), were selected to study shorter term responses to Al stress. POTCHETSTRM had higher callose synthase activity, lower ß-1,3-glucanase activity and more callose deposition in the root apices during Al treatment compared with ROMA. We monitored the expression of 12 genes involved in callose synthesis and degradation and found that one of these, SbGlu1 (Sb03g045630.1), which encodes a ß-1,3-glucanase enzyme, best explained the contrasting deposition of callose in ROMA and POTCHETSTRM during Al treatment. Full-length cDNAs of SbGlu1 was prepared from ROMA and POTCHETSTRM and expressed in Arabidopsis thaliana using the constitutive cauliflower mosaic virus (CaMV) 35S promoter. Independent transgenic lines displayed significantly greater Al tolerance than wild-type plants and vector-only controls. This phenotype was associated with greater total ß-1,3-glucanase activity, less Al accumulation and reduced callose deposition in the roots. These results suggest that callose production is not just an early indicator of Al stress in plants but likely to be part of the toxicity pathway that leads to the inhibition of root growth.

A quantum chemistry study on thermochemical properties of high energy-density endothermic hydrocarbon fuel JP-10.

The density functional theory (DFT) calculations at the M06-2X/6-31++G(d,p) level have been performed to explore the molecular structure, electronic structure, C-H bond dissociation enthalpy, and reaction enthalpies for five isodesmic reactions of a high energy-density endothermic hydrocarbon fuel JP-10. On the basis of the calculations, it is found that the carbonium ion C-6 isomer formed from the catalytic cracking at the C6 site of JP-10 has the lowest energy, and the R-5 radical generated from the thermal cracking at the C5 site of JP-10 is the most stable isomer. Furthermore, a series of hypothetical and isodesmic work reactions containing similar bond environments are used to calculate the reaction enthalpies for target compounds. For the same isodesmic reaction, the reaction enthalpy of each carbon site radical has also been calculated. The present work is of fundamental significance and strategic importance to provide some valuable insights into the component design and energy utilization of advanced endothermic fuels.

A DFT study on the thermal cracking of JP-10.

Density functional theory (DFT) calculations have been carried out to investigate the thermal cracking pathways of JP-10, a high energy density hydrocarbon fuel. Thermal cracking mechanisms are proposed, as supported by our previous experimental results (Xing et al. in Ind Eng Chem Res 47:10034-10040, 2008). Using DFT calculations, the potential energy profiles of the possible thermal cracking pathways for all of the diradicals obtained from homolytic C-C bond cleavage of JP-10 were derived and are presented here. The products of the different thermal cracking pathways are in good agreement with our previous experimental observations.

[Therapeutic effect and mechanism of sulfate polysaccharide of algae on lung cancer].

OBJECTIVE: To study the effect of sulfate polysaccharide of algae (SPA) on lung carcinoma and it's mechanism. METHODS: (1) C57BL/6 mice implanted with Lewis lung carcinoma were used as experimental animal model. The mice were randomly divided into a control group, SPA groups (3 groups) and a FT-207 group. After inoculation with Lewis lung carcinoma, the control group was treated with NS, the 3 SPA groups were treated with SPA 20 mg, 40 mg, and 80 mg/kg respectively, and the FT-207 group with FT-207 150 mg/kg for 10 days. The inhibiting activity of SPA on Lewis lung carcinoma was assayed, and proliferation of A549 tumor cells treated with SPA was detected by MTT assay. (2) New Zealand rabbits were randomly divided into a control group, a SPA 500 mg/kg group and a CTX 100 mg/kg group. Serum pharmacological method, and both in vivo and in vitro anti-tumor experiments were used in the study. After incubating A549 with SPA containing serum at different concentrations, the growth and apoptosis of cells, cell cycle, apoptosis rate and expression of apoptosis associated genes such as p53 and bcl-2 were detected by flow-cytometric assay. RESULTS: (1) SPA significantly inhibited the growth of implanted Lewis lung carcinoma in vivo and the effect had a dose dependent manner. The inhibitory rates of SPA on C57BL mice implanted Lewis lung carcinoma were 35.27% (P < 0.01), 48.29% (P < 0.01), and 65.41% (P < 0.01) respectively, which showed dose-dependent effects. SPA directly added to the culture medium neither induced A549 lung cancer cell apoptosis nor inhibited its proliferation in vitro. (2) SPA containing serum significantly induced A549 lung cancer cell apoptosis and inhibited its proliferation, with an increased expression of p53 and decreased expression of bcl-2 positive proteins, showing time and dose-dependent relationship. CONCLUSIONS: SPA possessed remarkable inhibitory activity against lung neoplasia in animal models and lung cancer cell strain. The anti tumor activity of SPA was considered to be derived from apoptosis induction, which might be associated with the increased expression of p53 and decreased expression of bcl-2 positive proteins.