In this paper, the multi-term time-fractional wave-diffusion equations are considered. The multi-term time fractional derivatives are defined in the Caputo sense, whose orders belong to the intervals [0,1], [1,2), [0,2), [0,3), [2,3) and [2,4), respectively. Some computationally effective numerical methods are proposed for simulating the multi-term time-fractional wave-diffusion equations. The numerical results demonstrate the effectiveness of theoretical analysis. These methods and techniques can also be extended to other kinds of the multi-term fractional time-space models with fractional Laplacian.
The genetic polymorphisms of biotransformation phase I enzymes, cytochrome P450 (CYP1A1 and CYP2D6), and phase II enzymes, glutathione S-transferase (GSTM1 and GSTT1), were analyzed in 204 healthy persons and 348 leukemia patients, who suffered from also acute lymphoblastic leukemia (ALL), acute nonlymphoblastic leukemia (ANLL) chronic myelogenous leukemia (CML), from the Han ethnic group in Changsha City of Hunan Province of China. Our results showed that the frequencies of polymorphisms of CYP1A1, CYP2D6 and GSTT1 among the groups including acute lymphoblastic leukemia, ANLL, chronic myelogenous leukemia and healthy control have no significant differences. The variation of GSTM1-null genotype alone correlated with the development of ANLL. The combined genotypes of GSTM1-null with GSTT1-null, or GSTM1-null with CYP1A1 heterozygous mutant, or GSTM1-null with CYP1A1 heterozygous mutant and CYP2D6 heterozygous mutant, or GSTM1-null with CYP1A1 heterozygous mutant, CYP2D6 heterozygous mutant and GSTT1-null were found in individuals with high risk of ANLL. All these findings suggest that GSTM1-null genotype alone or in coordination with the relevant genotypes of other metabolic enzymes might be susceptibility factors in the etiology of ANLL.
A case-control study was conducted for analyzing the genetic polymorphisms of phase II metabolic enzymes in 97 patients with lung cancer and 197 healthy subjects from Han ethnic group of Hunan Province located in Central South China. The results showed that the frequencies of glutathione S-transferase (GST) M1-null (GSTM1-) or GSTT1-null (GSTT1-) genotype alone, or combined form of both in lung cancer patients were significantly higher than those of the controls. Genotypes of combining GSTP1 mutant/GSTM1(-) or GSTP1 mutant/GSTT1(-) led to high risk of lung cancer. Individuals carrying any two or all three of GSTM1(-), GSTT1(-) and GSTP1 mutant genotypes have a distinctly increased risk of lung cancer when compared to those with GSTM1 present (GSTM1+: GSTM1+/+ or GSTM1+/−), GSTT1 present (GSTT1+: GSTT1+/+ or GSTT1+/−) and GSTP1 wild genotypes. Furthermore, individuals possessing combined genotypes of N-acetyltransferase 2 (NAT2) rapid acetylator, GSTP1 mutant and both GSTT1(-) and GSTM1(-) have a remarkably higher lung cancer risk than those carrying combined NAT2 slow acetylator genotype, GSTP1 wild genotype and both GSTT1(+) and GSTM1(+) genotypes. All these findings suggest that the genetic polymorphisms of phase II metabolic enzymes affect the susceptibility of lung cancer in the Han ethnic group of Central South China.
Aluminum (Al) is widespread in the environment including the ocean. The effects of Al on marine organisms have attracted more and more attention in recent years. However, the mechanisms of uptake of Al by marine organisms and the subcellular distribution of Al once assimilated are unknown. Here we report the uptake and subcellular distribution of Al in a marine diatom Thalassiosira weissflogii. Short-term (< 120 min) uptake experiments showed that the Al uptake rate by the diatom was 0.033 ± 0.013 fmol/cell/min (internalization flux normalized to the exposure Al concentration of 2 µM = 0.034 ± 0.013 nmol•m-2 •min-1 •nM-1). Subcellular fractionation experiments showed that the internalized Al was partitioned to subcellular components in the following order: granules (69 ± 5%) > debris (17 ± 4%) > organelles (12 ± 2%) > heat-stable peptides (HSP) (~2%) > heat-denaturable proteins (HDP) (< 1%), indicating that the majority of intracellular Al was detoxified and stored in inorganic forms. The subcellular distribution of Al in the diatom is different from that of Al in freshwater green algae, in which most of the internalized Al is partitioned to organelles. We also evaluated an artificial seawater-based EDTA rinse solution to remove Al adsorbed on the diatom cell surface. Overall, our study provides new information to understand the mechanisms of uptake of Al by marine diatoms, and the mechanisms responsible for the biological effects (both toxic and beneficial) of Al on the growth of marine phytoplankton, especially diatoms.
The risk factors in this study have the ability to identify patients with HMs and BSIs at high risk for mortality. Our model provides an excellent foundation for predicting 30-day morality in HM patients suffering from BSI and helps target high-risk patients for management decision making.
Recent studies indicate that aluminum (Al) could play an important role in the ocean carbon cycle by increasing phytoplankton carbon fixation and reducing organic carbon decomposition. However, how Al may influence the decomposition of organic carbon has not yet been explicitly examined. Here we report the effects of Al on carbon fixation by marine diatoms and their subsequent decomposition. By using radiocarbon as a tracer, the carbon fixation and decomposition of three model marine diatoms were examined in Aquil* media at different concentrations (0, 40, 200, and 2000 nM) of dissolved Al. Addition of Al enhanced net carbon fixation by the diatoms in the declining growth phase (by 9%-29% for Thalassiosira pseudonana, 15%-20% for T. oceanica, 15%-23% for T. weissflogii). Under axenic conditions the decomposition rates (d À1 ) of the diatomproduced particulate organic carbon (POC) significantly decreased (by 21%-57% for T. pseudonana, 0%-41% for T. oceanica, 29%-58% for T. weissflogii) in the Al-enriched treatments. In the presence of bacteria, the decomposition rates of T. weissflogii-produced POC were still 37%-38% lower in Al-enriched treatments compared to the control. Significant increases in cell size, cellular carbon content (pmol C/cell) and cellular carbon density (pmol C/μm 3 ) of T. weissflogii were also observed in the Al-enriched treatments compared to the control. The Al-related increase in net carbon fixation and cell size, and the decrease in POC decomposition rate may facilitate carbon export to ocean depths. The study provides new evidence for the iron-aluminum hypothesis, which suggests that Al could increase phytoplankton uptake of atmospheric CO 2 and influence climate change.
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