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As a green and economic emerging technology, biological desulfurization is popular. However, biological desulfurization is inhibited by organosulfur in the treatment gases which cannot be ignored. This article summarizes relevant studies on the influence of organosulfur on biological desulfurization in recent years, including the types and physicochemical characteristics of organosulfur, the influence of organosulfur on the desulfurization process, the reaction mechanism of organosulfur, the interplay between organosulfur and some operating conditions, and species of microorganisms that are tolerant to organosulfur. Methods for mitigating the effect of organosulfur on the desulfurization process are discussed, to provide references for the stable and efficient operation of biological desulfurization.
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Biological desulfurization is a process in which sulfur compounds are removed from gas and oil using microorganisms. It is a simple process that has mild operating conditions, high desulfurization efficiency, low energy consumption and less environmental pollution. However, there is still a lack of simple and efficient analytical methods for quantitatively analyzing the sulfur compounds in the biological desulfurization process. In order to solve this problem, the analytical method for the simultaneous determination of sulfite, thiosulfate and sulfide in biological desulfurization solutions by pre-column fluorescence derivation using high performance liquid chromatography (HPLC) was developed. The standard curves of sulfur species in this analytical method had good linear relationships with correlation coefficients of 0.999 5, 0.999 7, and 0.999 7 for sulfite, thiosulfate and sulfide, respectively. The detection limits of these sulfur compounds were 0.000 6, 0.000 7 and 0.001 1 μmol/L; the range of recovery rates were 98.17 to 101.9%, 100.9 to 102.6%, and 101.1 to 104.2%; which had good repeatability and stability. The analytical method was simple, efficient and accurate, and could be used to simultaneously determine the sulfur compounds in different biological desulfurization systems.
Subject(s)
Chemistry Techniques, Analytical/methods , Chromatography, High Pressure Liquid , Sulfur Compounds/analysisABSTRACT
Malic acid is widely used in food, and chemical industries. Through overexpressing pyruvate carboxylase and malate dehydrogenase in pdc1-deficient Saccharomyces cerevisiae, malic acid was successfully produced through the reductive TCA pathway. No malic acid was detected in wild type Saccharomyces cerevisiae, however, 45 mmol/L malic acid was produced in engineered strain, and the concentration of byproduct ethanol also reduced by 18%. The production of malic acid enhanced 6% by increasing the concentration of Ca2+. In addition, the final concentration reached 52.5 mmol/L malic acid by addition of biotin. The increasing is almost 16% higher than that of the original strain.
Subject(s)
Citric Acid Cycle , Fermentation , Industrial Microbiology , Methods , Malate Dehydrogenase , Genetics , Metabolism , Malates , Metabolism , Metabolic Engineering , Methods , Metabolic Networks and Pathways , Oxidation-Reduction , Pyruvate Carboxylase , Genetics , Metabolism , Saccharomyces cerevisiae , Genetics , Metabolism , Signal TransductionABSTRACT
Objective To explore the influencing factors and possible mechanism of osteonecrosis of the femoral head(ONFH)in patients with leukemia after allogeneic hematopoietic stem cell transplantation (Allo-HSCT).Methods One hundred and two patients with leukemia who received Allo-HSCT between January 2003 and October 2007 were evaluated for ONFH and graft-versus-host disease(GvHD)within 2years after transplantation,and the dosage of methylprednisolone(MP)in every patient from the first diagnosis of leukemia to 2 years after Allo-HSCT was calculated.For patients who suffered acute GvHD(aGvHD) and chronic GvHD(cGvHD),the serum leveh of soluble ligand of receptor activator of nuclear factor kappa B (sRANKL)which was index for differentiation of osteoclast(OC),tartrate-resistant acid phosphatase-5b(TRAP-5b)and C-terminal telopeptide of collagen Ⅰ(CTP-Ⅰ)which both were indexes for metabolism of OC were detected by enzyme-linked immunosorbent assay in different stages of MP dosage.According to these results.possible factors for ONFH after Allo-HSCT were analyzed.Results Seven in 102 patients after Allo-HSCT had experienced ONFH within 2 years,the incidence was 6.9%(7/102),which was not related to age,gender,types of leukemia and donor.ONFH mainly developed in patients with aGvHD and cGvHD,and the incidence could be achieved to 21.9%(7/32)which Was much higher than that in patients with no GvHD,merely aGvHD or merely cGvHD(P<0.05).In patients with aGvHD and cGvHD,the average dosage of MP in ONFH(+)was(232.7±28.6)mg/kg which was extremely higher than that in ONFH(-)(115.1±16.9)mg/kg(P<0.05).The serum levels of sRANKL,TRAP-5b and CTP-Ⅰ were also higher when ONFH happened than ahead of pretreatment and 28 days after transplantation(-)(P<0.05),and they were closely related to the dosage of MP(correlation coefficient was 0.597,0.664 and 0.682 respectively,P<0.05).Conclusions After Allo-HSCT,ONFH is related to the dosage of MP in treatment of GvHD.MP may be responsible for enhancement of OC differentiation and metabolism in leukemia patients,and ultimately induced the onset of ONFH.
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Objective To investigate the effect of bortezomib on the proliferation and apoptosis in leukemia cell line NB_4-R2 in vitro and provide some new evidences for the treatment of acute promyelocytic leukemia APL with ATRA-resistant using bortezomib. Methods NB_4-R2 cells were incubated with bortezomib at different does for 48 h. The proliferation capacity was measured by MTT assay, the morphology of cell apoptosis observed with Hoechst33342 staining by fluorescence microscopy and the percentage of apoptosis calculated by flow cytometry. The expression of apoptosis protein of cleaved (poly ADP-ribose polymerase, PARP) and Caspase-3 were determined by Western blotting. Results The proliferation of NB_4-R2 cells were obviously inhibited by bortezomib in vivo and the role of inhibition was a does-dependant manner within the scope of the bortezomib concentration from 1-5 μg /L.The incidence of inhibition was up to 74.9 % at the bortezomib concentration of 5 μg/L. Within this scope of the bortezomib concentration mentioned above, the role of inhibition of proliferation of NB_4-R2 cells mainly showed an increase of the late apoptosis, and the percentage of apoptosis was up to 78.9 %. In the meaning time, the expressions of the apoptotic protein of cleaved PARP and Caspase-3 were up-regulated in NB_4-R2 cells after treated with bortezomib by Western blotting assay. Conclusion Bortezomib can inhibit the proliferation of NB_4-R2 cells in vivo by inducing cell apoptosis.
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AIM: To re-identify the special motif regulating osteoclast(OC)differentiation in receptor activator of nuclear factor kappa B(RANK)to provide evidences for studying the mechanism of OC differentiation.METHODS: Eight amino acids were mutated(from DIIVVYVS into ELLAAFAA)in the fragment between the 533th and the 540th amino acids in RANK cytoplasmic domain.Eight mutant TNFR1/RANK chimeras,each consists of TNFR1(tumor necrosis factor receptor 1)extracellular domain linked to transmembrane domain and cytoplasmic domain of RANK with one amino acid mutated in cytoplasmic domain was constructed by point mutation method.After the eight mutant chimeras were finished,they were packed with plat E cell line to produce the retrovirus expressing mutant TNFR1/RANK.The bone marrow macrophages(BMMs),isolated from TNFR1/R2 double knockout mice,were infected with retrovirus derived from different mutants and infected BMMs which did not differentiated into OCs were inspected after stimulated by TNF-? and M-CSF.The fragment consisted of different amino acids in TNFR1/RANK chimeras,which couldn't induce OC formation after mutated,may be the special motif regulating OC differentiation.RESULTS: We found that all BMMs transfected by TNFR1/RANK-533,TNFR1/RANK-539 or TNFR1/RANK-540 differentiated into OCs,indicating that none of amino acids D533,V539 or S540 had an effect on OC differentiation.A fewer of BMMs transfected by TNFR1/RANK-534 differentiated into OCs,indicating that I534 had a partial effect on OC formation.Most importantly,BMMs transfected TNFR1/RANK-535,TNFR1/RANK-536,TNFR1/RANK-537 or TNFR1/RANK-538 did not differentiated into OCs,indicating each of amino acids I535,V536,V537 and Y538 played a pivotal role in OC differentiation.CONCLUSION: The amino acid fragment consists of I534,I535,V536,V537 and Y538 may be the special motif regulating OC differentiation in RANK.