Numerička studija izrađena pomoću ChemKin za rasplinjavanje vodene pare ugljene prašine i transformacije žive unutar rasplinjača s vodenom parom

Zero-emission coal (ZEC) technology has been actively studied recently. It aims to achieve zero emission of CO2 and other pollutants and the efficiency of this system can reach no less than 70%. Hydro-gasification of pulverized coal is a core process of ZEC. However, the mechanism of gasification and transformation of mercury speciation in the hydro-gasification is has not been understood precisely up until now. This restrains the ZEC’s commercialization. The purpose of this paper is to study the mechanism of hydro-gasification and mercury speciation transformation for coal in the gasifier with high temperature and pressure. Detailed chemical kinetics mechanism (CKM) has been proposed for hydro-gasification for pulverized coal in an entrained flow hydro-gasifier. The effects have been studied for different reaction conditions on hydro-gasification products and evolution of Hg in terms of the chemical reaction kinetics method. The CKM mechanism includes 130 elementary reactions and is solved with commercially available software, ChemKin. The calculation results are validated against the experimental data from literature and meaningful predictions are finally obtained. In addition, the chemical equilibrium calculation (CEC) is also used for predictions. Although the CEC method assumes all the reactions have reached chemical equilibrium, which is not the case in industrial reality, the calculation results are of value as reference.Tehnologija korištenja ugljena bez emisija (ZEC) se od nedavno aktivno proučava. Njezin cilj je postizanje nulte stope emisija CO2 te ostalih štetnih tvari dok efikasnost sustava mora biti minimalno 70%. Rasplinjavanje ugljene prašine vodenom parom je temeljni proces ZEC-a. Međutim, mehanizam rasplinjavanja i transformacije žive u rasplinjavanju vodenom parom još nije u potpunosti shvaćeno. To ograničava mogućnost komercijalne primjene ZEC-a. Cilj ovog rada je proučavanje mehanizama rasplinjavanja vodenom parom i transformacije žive za rasplinjavanje ugljena u rasplinjaču s visokim temperaturama i tlakom. Predloženi su detaljni kemijski kinetički mehanizmi (CKM) za rasplinjavanje ugljene prašine u fluidiziranom sloju sa zajedničkim tokom tvari. Proučeni su utjecaji raznih uvjeta pod kojim su se odvijale reakcije na produkte rasplinjavanja i evoluciju žive u uvjetima kemijskih reakcija kinetičke metode. CMK mehanizam sadrži 130 elementarnih reakcija i rješava se s komercijalno dostupnim programom, ChemKin. Rezultati simulacije se uspoređuju s eksperimentalnim iz literature te su konačno dobivena smislena predviđanja. Jednadžbe kemijske ravnoteže (CEC) su također korištene za predviđanja. Iako CEC metoda pretpostavlja da su sve reakcije postigle ravnotežu, što nije uvijek slučaj u industriji, rezultati tog proračuna mogu poslužiti kao referenca

A New Behavior of Nuclei during Mitosis of Lilium Hybrids

Mitosis is nuclear division plus cytokinesis,and produces two identical daughter cells during prophase, prometaphase, metaphase, anaphase, and telophase. However, a new nucleus behavior in interspecific hybrid progenies of Lilium was observed in our experiment. Very unusual behaviors of nuclei surprisingly presented during the mitosis, such as sprouting or germination, tube-like elongation, penetrating cell membrane into a neighbor cell, the top of nuclei tube expanding, intruding and splitting of the tube-like nucleus, and micronucleus formation, and so on. Furthermore, the tetrad of meiosis was founded in mitosis of root.

Routine of the unusual nucleus behaviors observed in our experiment may be summarized as nucleus germination¬— tube-like elongation— penetrating cell membrane— entering a neighbor cell—the top of nuclei tube expanding—tube ingression and splitting— formation of a new nucleus or micronucleus.

Many kinds of abnormal mitosis caused by chemical and physical induction such as unequal division, chromosome bridges, lagging chromosomes, and multiple nuclei have resulted in variations of chromosome number and structure. However, this new nucleus behavior is firstly reported, these phenomena implied that the DNA maybe easily emigrates from one cell to another. Therefore, the unusual behaviors of nuclei in hybrid progenies of Lilium not only create mutations for breeding of new cultivars, also produce possibly ideal materials for exotic DNA or gene transfication with simple method in meristem. This mode of nuclei behaviors is a new addition to cytogenetics of plant of vegetative propagation and provide a new genetic mechanism of species evolution from interspecific hybridization

Sam50 Regulates PINK1-Parkin-Mediated Mitophagy by Controlling PINK1 Stability and Mitochondrial Morphology

PINK1 and Parkin mediate mitophagy, the cellular process that clears dysfunctional mitochondria. Mitophagy is regulated by mitochondrial dynamics, but the molecules linking these two processes remain poorly understood. Here, we show that Sam50, the core component of the sorting and assembly machinery (SAM), is a critical regulator of mitochondrial dynamics and PINK1-Parkin-mediated mitophagy. In response to Sam50 depletion, normal tubular mitochondria are first fragmented and subsequently merged into large spheres. Sam50 interacts with PINK1 to facilitate its processing and degradation. Depletion of Sam50 results in PINK1 accumulation, Parkin recruitment, and mitophagy. Interestingly, Sam50 deficiency induces a piecemeal mode of mitophagy that eliminates mitochondria “bit by bit” but spares mtDNA. In C. elegans, the Sam50 homolog gop-3 is required for the maintenance of mitochondrial morphology and mass. Our findings reveal that Sam50 directly links mitochondrial dynamics and mitophagy and that Sam50 depletion induces elimination of mitochondria without affecting mtDNA content

Transcriptome analysis reveals salt-stress-regulated biological processes and key pathways in roots of cotton (Gossypium hirsutum L.)

AbstractHigh salinity is one of the main factors limiting cotton growth and productivity. The genes that regulate salt stress in TM-1 upland cotton were monitored using microarray and real-time PCR (RT-PCR) with samples taken from roots. Microarray analysis showed that 1503 probe sets were up-regulated and 1490 probe sets were down-regulated in plants exposed for 3h to 100mM NaCl, and RT-PCR analysis validated 42 relevant/related genes. The distribution of enriched gene ontology terms showed such important processes as the response to water stress and pathways of hormone metabolism and signal transduction were induced by the NaCl treatment. Some key regulatory gene families involved in abiotic and biotic sources of stress such as WRKY, ERF, and JAZ were differentially expressed. Our transcriptome analysis might provide some useful insights into salt-mediated signal transduction pathways in cotton and offer a number of candidate genes as potential markers of tolerance to salt stress

FDXR drives primary and endocrine-resistant tumor cell growth in ER+ breast cancer via CPT1A-mediated fatty acid oxidation

Background The majority of breast cancers (BCs) expressing estrogen receptor (ER) have shown endocrine resistance. Our previous study demonstrated that ferredoxin reductase (FDXR) promoted mitochondrial function and ER+ breast tumorigenesis. But the underlying mechanism is not clear. Methods Liquid chromatography (LC) tandem mass spectrometry (MS/MS)-based metabolite profiling was utilized to reveal the metabolites regulated by FDXR. RNA microarray was utilized to determine the potential downstream targets of FDXR. Seahorse XF24 analyzer was performed to analyze the FAO-mediated oxygen consumption rate (OCR). Q-PCR and western blotting assays were used to measure expression levels of FDXR and CPT1A. MTS, 2D colony formation and anchorage-independent growth assays were used to evaluate the effects of FDXR or drug treatments on tumor cell growth of primary or endocrine-resistant breast cancer cells. Results We found that depletion of FDXR inhibited fatty acid oxidation (FAO) by suppressing CPT1A expression. Endocrine treatment increased the expression levels of both FDXR and CPT1A. Further, we showed that depletion of FDXR or FAO inhibitor etomoxir treatment reduced primary and endocrine-resistant breast cancer cell growth. Therapeutically, combining endocrine therapy with FAO inhibitor etomoxir synergistically inhibits primary and endocrine-resistant breast cancer cell growth. Discussion We reveal that the FDXR-CPT1A-FAO signaling axis is essential for primary and endocrine-resistant breast cancer cell growth, thus providing a potential combinatory therapy against endocrine resistance in ER+ breast cancer

FDXR drives primary and endocrine-resistant tumor cell growth in ER+ breast cancer via CPT1A-mediated fatty acid oxidation

BackgroundThe majority of breast cancers (BCs) expressing estrogen receptor (ER) have shown endocrine resistance. Our previous study demonstrated that ferredoxin reductase (FDXR) promoted mitochondrial function and ER+ breast tumorigenesis. But the underlying mechanism is not clear.MethodsLiquid chromatography (LC) tandem mass spectrometry (MS/MS)-based metabolite profiling was utilized to reveal the metabolites regulated by FDXR. RNA microarray was utilized to determine the potential downstream targets of FDXR. Seahorse XF24 analyzer was performed to analyze the FAO-mediated oxygen consumption rate (OCR). Q-PCR and western blotting assays were used to measure expression levels of FDXR and CPT1A. MTS, 2D colony formation and anchorage-independent growth assays were used to evaluate the effects of FDXR or drug treatments on tumor cell growth of primary or endocrine-resistant breast cancer cells.ResultsWe found that depletion of FDXR inhibited fatty acid oxidation (FAO) by suppressing CPT1A expression. Endocrine treatment increased the expression levels of both FDXR and CPT1A. Further, we showed that depletion of FDXR or FAO inhibitor etomoxir treatment reduced primary and endocrine-resistant breast cancer cell growth. Therapeutically, combining endocrine therapy with FAO inhibitor etomoxir synergistically inhibits primary and endocrine-resistant breast cancer cell growth.DiscussionWe reveal that the FDXR-CPT1A-FAO signaling axis is essential for primary and endocrine-resistant breast cancer cell growth, thus providing a potential combinatory therapy against endocrine resistance in ER+ breast cancer

The Paf1 complex transcriptionally regulates the mitochondrial-anchored protein Atg32 leading to activation of mitophagy

Mitophagy is a critical process that safeguards mitochondrial quality control in order to maintain proper cellular homeostasis. Although the mitochondrial-anchored receptor Atg32-mediated cargo-recognition system has been well characterized to be essential for this process, the signaling pathway modulating its expression as a contribution of governing the mitophagy process remains largely unknown. Here, bioinformatics analyses of epigenetic or transcriptional regulators modulating gene expression allow us to identify the Paf1 complex (the polymerase-associated factor 1 complex, Paf1C,) as a transcriptional repressor of ATG genes. We show that Paf1C suppresses glucose starvation-induced autophagy, but does not affect nitrogen starvation- or rapamycin-induced autophagy. Moreover, we show that Paf1C specifically regulates mitophagy through modulating ATG32 expression. Deletion of the genes encoding two core subunits of Paf1C, Paf1 and Ctr9, increases ATG32 and ATG11 expression and facilitates mitophagy activity. Although Paf1C is required for many histone modifications and gene activation, we show that Paf1C regulates mitophagy independent of its positive regulatory role in other processes. More importantly, we also demonstrate the mitophagic role of PAF1C in mammals. Overall, we conclude that Paf1C maintains mitophagy at a low level through binding the promoter of the ATG32 gene in glucose-rich conditions. Dissociation of Paf1C from ATG32 leads to the increased expression of this gene, and mitophagy induction upon glucose starvation. Thus, we uncover a new role of Paf1C in modulating the mitophagy process at the transcriptional level

Serum CHI3L1 as a biomarker of interstitial lung disease in rheumatoid arthritis

BackgroundInterstitial lung disease (ILD) is a relatively prevalent extra-articular manifestation of rheumatoid arthritis (RA) and contributes to significant morbidity and mortality. This study aimed to analyze the association between chitinase-3 like-protein-1(CHI3L1) and the presence of RA-ILD.MethodsA total of 239 RA patients fulfilling the American Rheumatism Association (ACR) 1987 revised criteria were enrolled and subclassified as RA-ILD and RA-nILD based on the results of high-resolution computed tomography scans (HRCT) of the chest. The disease activity of RA was assessed by Disease Activity Score for 28 joints (DAS28) and categorized as high, moderate, low, and remission. Chemiluminescence immunoassays were applied to determine the serum levels of CHI3L1. Univariate analysis was performed and the receiver operating characteristics (ROC) curves were plotted to evaluate the correlation between RA-ILD and CHI3L1.ResultsAmong the eligible RA patients studied, 60 (25.1%) patients were diagnosed with RA-ILD. Compared with RA-nILD, RA patients with ILD had significantly higher median age (median [IQR], 68.00 [62.00-71.75] vs 53.00 [40.00-63.00], p<0.001) and a higher proportion of males (21 (35.0%) vs 30 (16.8%), p=0.003). Notably, differences in DAS28 scores between the two groups were not observed. The serum level of CHI3L1 was significantly higher in RA-ILD patients (median [IQR], 69.69 [44.51-128.66] ng/ml vs 32.19 [21.63-56.99] ng/ml, p<0.001). Furthermore, the areas under the curve (AUC) of CHI3L1 attained 0.74 (95% confidence interval [CI], 0.68-0.81, p<0.001) in terms of identifying patients with RA-ILD from those without ILD. Similar trends were seen across the spectrum of disease activity based on DAS28-ESR.ConclusionOur findings of elevated serum CHI3L1 levels in RA-ILD patients suggest its possible role as a biomarker to detect RA-ILD noninvasively

Climate change : strategies for mitigation and adaptation

The sustainability of life on Earth is under increasing threat due to humaninduced climate change. This perilous change in the Earth's climate is caused by increases in carbon dioxide and other greenhouse gases in the atmosphere, primarily due to emissions associated with burning fossil fuels. Over the next two to three decades, the effects of climate change, such as heatwaves, wildfires, droughts, storms, and floods, are expected to worsen, posing greater risks to human health and global stability. These trends call for the implementation of mitigation and adaptation strategies. Pollution and environmental degradation exacerbate existing problems and make people and nature more susceptible to the effects of climate change. In this review, we examine the current state of global climate change from different perspectives. We summarize evidence of climate change in Earth’s spheres, discuss emission pathways and drivers of climate change, and analyze the impact of climate change on environmental and human health. We also explore strategies for climate change mitigation and adaptation and highlight key challenges for reversing and adapting to global climate change