Biosynthesis of xanthan gum on wastewater from confectionary industry

Xanthan gum is one of the major commercial biopolymers employed in many industrial processes owing to its unique physical properties such as a high degree of pseudoplasticity and high viscosity even at low concentrations. Commercially available xanthan gum is relatively expensive due to glucose or sucrose being used as the sole carbon source for its production and cost reduction could be achieved by using less expensive substrates, such as food industrial wastewaters. Effluents from the confectionery industry, because of its high organic content, are significant environmental pollutants and before their release into environment it is necessary to purify them. The present study examines xanthan production by Xanthomonas campestris under aerobic conditions on wastewaters from five different factories of the confectionery industry. Xanthan yield was obtained as a quantitative characteristic of the process and was in the range between 4.28 g/L and 10.03 g/L and its quality is determined by following rheological characteristics of obtained cultivation media. The results obtained in this study indicate that wastewater from confectionary industry can be used as the basis of media for the production of this highly valuable product

Optimization of media for antimicrobial compounds production by Bacillus subtilis

Bacillus subtilis is one of the most important producers of diverse antimicrobial compounds. This bacterium grows and produces antibiotics on different substrates. The increase of the antibiotics yield can be achieved by changing the conditions of cultivation and the composition of the culture media. In this study, response surface methodology was used for optimization of glycerol, sodium nitrite, and phosphate content in media for production of antibiotics effective against Staphylococcus aureus. As biosynthesis strain Bacillus subtilis ATCC 6633 was used. The developed model predicts that the maximum inhibition zone radius (38.08 mm) against Staphylococcus aureus and minimal amount of residual nutrients (glycerol 1.75 g l−1, nitrogen 0.21 g l−1, phosphorus 0.18 g l−1) are achieved, when the initial content of glycerol, sodium nitrite, and phosphate are 49.99 g l−1, 1.00 g l−1, and 5.00 g l−1, respectively

Chronic high fat diet intake impairs hepatic metabolic parameters in ovariectomized Sirt3 KO mice

High fat diet (HFD) is an important factor in the development of metabolic diseases, with liver as metabolic center being highly exposed to its influence. However, the effect of HFD-induced metabolic stress with respect to ovary hormone depletion and sirtuin 3 (Sirt3) is not clear. Here we investigated the effect of Sirt3 in liver of ovariectomized and sham female mice upon 10 weeks of feeding with standard-fat diet (SFD) or HFD. Liver was examined by Folch, gas chromatography and lipid hydroperoxide analysis, histology and oil red staining, RT-PCR, Western blot, antioxidative enzyme and oxygen consumption analyses. In SFD-fed WT mice, ovariectomy increased Sirt3 and fatty acids synthesis, maintained mitochondrial function, and decreased levels of lipid hydroperoxides. Combination of ovariectomy and Sirt3 depletion reduced pparα, Scd-1 ratio, MUFA proportions, CII-driven respiration, and increased lipid damage. HFD compromised CII-driven respiration and activated peroxisomal ROS scavenging enzyme catalase in sham mice, whereas in combination with ovariectomy and Sirt3 depletion, increased body weight gain, expression of NAFLD- and oxidative stress-inducing genes, and impaired response of antioxidative system. Overall, this study provides evidence that protection against harmful effects of HFD in female mice is attributed to the combined effect of female sex hormones and Sirt3, thus contributing to preclinical research on possible sex-related therapeutic agents for metabolic syndrome and associated diseases

The Tongue Squamous Carcinoma Cell Line Cal27 Primarily Employs Integrin α6β4-Containing Type II Hemidesmosomes for Adhesion Which Contribute to Anticancer Drug Sensitivity

Integrins are heterodimeric cell surface glycoproteins used by cells to bind to the extracellular matrix (ECM) and regulate tumor cell proliferation, migration and survival. A causative relationship between integrin expression and resistance to anticancer drugs has been demonstrated in different tumors, including head and neck squamous cell carcinoma. Using a Cal27 tongue squamous cell carcinoma model, we have previously demonstrated that de novo expression of integrin αVβ3 confers resistance to several anticancer drugs (cisplatin, mitomycin C and doxorubicin) through a mechanism involving downregulation of active Src, increased cell migration and invasion. In the integrin αVβ3 expressing Cal27-derived cell clone 2B1, αVβ5 expression was also increased, but unrelated to drug resistance. To identify the integrin adhesion complex (IAC) components that contribute to the changes in Cal27 and 2B1 cell adhesion and anticancer drug resistance, we isolated IACs from both cell lines. Mass spectrometry (MS)-based proteomics analysis indicated that both cell lines preferentially, but not exclusively, use integrin α6β4, which is classically found in hemidesmosomes. The anticancer drug resistant cell clone 2B1 demonstrated an increased level of α6β4 accompanied with increased deposition of a laminin-332-containing ECM. Immunofluorescence and electron microscopy demonstrated the formation of type II hemidesmosomes by both cell types. Furthermore, suppression of α6β4 expression in both lines conferred resistance to anticancer drugs through a mechanism independent of αVβ3, which implies that the cell clone 2B1 would have been even more resistant had the upregulation of α6β4 not occurred. Taken together, our results identify a key role for α6β4-containing type II hemidesmosomes in regulating anticancer drug sensitivity