RESUMO
This paper addresses the issue of combining the usage of waste frying oil (WFO), as a feedstock, and a lipase produced in solid-state fermentation (SSF), as a biocatalyst, for semi-pilot scale production of biodiesel as fatty acid methyl esters (FAME). Two fungal mutants namely; Rhizopus stolonifer 1aNRC11 mutant F (1F) and Aspergillus tamarii NDA03a mutant G (3G) were used as a cocatalyst. The two mutants were cultivated separately by SSF in a tray bioreactor. The dried fermented solid of 1F and 3G mutants were used in a ratio of 3:1, respectively, for WFO transesterification. Optimization of several semi-pilot process stages including SSF and WFO transesterification reaction conditions resulted in 92.3% conversion of WFO to FAME. This FAME yield was obtained after 48 h using 10% cocatalyst (w/w of WFO), 10% water (w/w of WFO) and 3:1 methanol/ WFO molar ratio at 30 °C and 250 rpm. A preliminary economic evaluation of produced biodiesel price (190 $/Ton) is less than half the price of petroleum diesel in Egypt (401$/Ton) and is about 40.3% the price of biodiesel produced using a pure enzyme, which is a promising result. This strategy makes the biodiesel synthesis process greener, economical and sustainable.
Assuntos
Aspergillus/metabolismo , Biocombustíveis , Proteínas Fúngicas/metabolismo , Lipase/metabolismo , Óleos de Plantas/metabolismo , Rhizopus/metabolismo , Aspergillus/genética , Aspergillus/crescimento & desenvolvimento , Biocombustíveis/análise , Biocombustíveis/microbiologia , Reatores Biológicos/microbiologia , Esterificação , Fermentação , Proteínas Fúngicas/genética , Lipase/genética , Mutação , Rhizopus/genética , Rhizopus/crescimento & desenvolvimentoRESUMO
BACKGROUND: In our previous work, we provided strong evidence that nucleophosmin (NPM) gene mutation has an important role in leukemogenesis of primary acute myeloid leukemia (AML). Furthermore, we speculated a new targeted therapy in patients with primary AML and bearing mutated NPM (mNPM). Based on these results together with findings of other researchers, it was essential to develop a method for accurate detection of mNPM. METHODS: Our method based on utilizing the most recent flow cytometeric techniques and instruments in measuring mNPM. Attributed to their availability and technical feasibility, we used human leukemia cell lines to validate our method. RESULTS: The main findings were differential expression of wild-type NPM (wtNPM) within the same sample. Furthermore flow cytometry (FCM) was a simple straightforward tool for quantitative assay of mNPM. CONCLUSIONS: In this work we developed an innovative technique that could enable quantitative assay of mNPM, and ease its use as a biomarker in cytogenetic and molecular prognostication of primary AML. In addition the study suggested that FCM could differentiate mNPM expression within cells of the same patient thus could be used for monitoring of minimal residual disease.
RESUMO
BACKGROUND: Acute myeloid leukemia (AML) is a hematopoietic stem cell disorder that carries very poor prognosis. Understanding molecular basis of AML leukemogenesis could lead to the emergence of effective targeted therapies for AML. AML bearing nucleophosmin (NPM) gene mutation has distinct features. This study was conducted to investigate the role of mutated (m) NPM in pathogenesis of de novo AML through studying its contribution in proliferation of AML cell line cells. METHODS: Two types of human leukemia cell lines were used. One of them was a model for AMLs with mNPM and the other for AMLs with wild type (wt) NPM. Assessment of the proliferative role of mNPM in AML was carried out using cell culture and viability studies. The obtained results were reaffirmed by immunocytochemical and immunoblotting techniques. RESULTS: Analysis of results was done with the appropriate computer software. It showed higher proliferative potential of cells with mNPM compared to those bearing wtNPM only. Furthermore, the immunocytochemical studies demonstrated subcellular localization of NPM isoforms during various phases of mitosis. Mitosis was associated with cytoplasmic translocation of wtNPM in certain phases, while localization of mNPM remained unchanged throughout the cell cycle. Results of immunoblotting showed little or no change in protein expression of either NPM moieties during mitosis. CONCLUSIONS: The current study demonstrated important contribution of NPM gene mutation in enhancing proliferation of AML cell lines. These results confirmed the role of mNPM in AML leukemogenesis, and highlighted the importance of targeting mNPM in new evolving AML therapies.
RESUMO
To determine the patterns of thyroid dysfunction and autoantibodies associated with SLE and RA patients, twenty patients with SLE and another group of twenty with RA were studied. The results were compared with those of twenty apparently healthy age- and sex- matched controls. All patients were subjected to complete history taking, thorough clinical examination and joint examination. All patients and controls were subjected to the following investigations: T3, T4, TSH, antithyroglobulin antibodies (ATGAb) and thyroid peroxidase antibodies (TPOAb). Also, complete blood picture, ESR, RF, ANA, CRP and LE cells were done. This study revealed that thyroid disorders were significantly increased in SLE patients (50%) when compared to RA (15%) (P<0.05). In SLE group, 20% had euthyroid sick syndrome, 20% had hypothyroidism (10% subclinical and 10% biochemical), and 10% had hyperthyroidism (5% subclinical and 5% biochemical). However, in RA, 10% had hypothyroidism (subclinical) and 5% had subclinical hyperthyroidism. TPOAb was found in 15% of SLE and 5% of RA patients and 10% of controls, but the titres were higher in SLE and RA patients. Also, ATGAb was found in 5% of SLE, 30% of RA patients and 10% of controls, but the titres were higher in SLE and RA patients. It is concluded that thyroid abnormalities are more implicated with euthyroid sick syndrome and hypothyroidism (subclinical and overt) than hyperthyroidism in SLE patients. SLE and RA were associated with antithyroid antibodies (TPOAb in SLE and ATGAb in RA). Performance of thyroid function tests in patients with SLE, in particular and RA as a part of the biochemical and immunological profiles, may help in early detection of associated thyroid disorders.