Potential of Marine-Derived Fungi to Remove Hexavalent Chromium Pollutant from Culture Broth

Chromium (Cr) released from industrial units such as tanneries, textile and electroplating industries is detrimental to the surrounding ecosystems and human health. The focus of the present study was to check the Cr(VI) removal efficiency by marine-derived fungi from liquid broth. Amongst the three Cr(VI) tolerant isolates, #NIOSN-SK56-S19 (Aspergillus sydowii) showed Cr-removal efficiency of 0.01 mg Cr mg^?1 biomass resulting in 26% abatement of total Cr with just 2.8 mg of biomass produced during the growth in 300 ppm Cr(VI). Scanning Electron Microscopy revealed aggregation of mycelial biomass with exopolysaccharide, while Electron Dispersive Spectroscopy showed the presence of Cr₂O₃ inside the biomass indicating presence of active Cr(VI) removal mechanisms. This was further supported when the Cr(VI) removal was monitored using DPC (1,5-diphenylcarbazide) method. The results of this study point to the potential of marine-derived fungal isolates for Cr(VI) removal.     

On principles and standards in ecological restoration

The Society for Ecological Restoration (SER) has long debated how to define best practices. We argue that a principles‐first approach offers more flexibility for restoration practitioners than a standards‐based approach, is consistent with the developmental stage of restoration, and functions more effectively at a global level. However, the solution is not as simple as arguing that one approach to professional practice is sufficient. Principles and standards can and do operate effectively together, but only if they are coordinated in a transparent and systematic way. Effective professional guidance results when standards anchored by principles function in a way that is contextual and evolving. Without that clear relation to principles, the tendency to promote performance standards may lead to a narrowing of restoration practice and reduction in the potential to resolve very difficult and diverse ecological and environmental challenges. We offer recommendations on how the evolving project of restoration policy by SER and other agencies and organizations can remain open and flexible.     

Comparison of Two Mathematical Models of Cellularity Calculation

OBJECT: Nowadays, there is increasing evidence that functional magnetic resonance imaging (MRI) modalities, namely, diffusion-weighted imaging (DWI) and dynamic-contrast enhanced MRI (DCE MRI), can characterize tumor architecture like cellularity and vascularity. Previously, two formulas based on a logistic tumor growth model were proposed to predict tumor cellularity with DWI and DCE. The purpose of this study was to proof these formulas. METHODS: 16 patients with head and neck squamous cell carcinomas were included into the study. There were 2 women and 14 men with a mean age of 57.0 ± 7.5 years. In every case, tumor cellularity was calculated using the proposed formulas by Atuegwu et al. In every case, also tumor cell count was estimated on histopathological specimens as an average cell count per 2 to 5 high-power fields. RESULTS: There was no significant correlation between the calculated cellularity and histopathologically estimated cell count by using the formula based on apparent diffusion coefficient (ADC) values. A moderate positive correlation (r=0.515, P=.041) could be identified by using the formula including ADC and V_e values. CONCLUSIONS: The formula including ADC and V_e values is more sensitive to predict tumor cellularity than the formula including ADC values only.     

Pregna-5,17(20)-dien-21-oyl amides affecting sterol and triglyceride biosynthesis in Hep G2 cells

Synthesis of series [17(20)Z]- and [17(20)E]-pregna-5,17(20)-dien-21-oyl amides, containing polar substituents in amide moiety, based on rearrangement of 17α-bromo-21-iodo-3β-acetoxypregn-5-en-20-one caused by amines, is presented. The titled compounds were evaluated for their potency to regulate sterol and triglyceride biosynthesis in human hepatoma Hep G2 cells in comparison with 25-hydroxycholesterol. Three [17(20)E]-pregna-5,17(20)-dien-21-oyl amides at a concentrations of 5 μM inhibited sterol biosynthesis and stimulated triglyceride biosynthesis; their regulatory potency was dependent on the structure of amide moiety; the isomeric [17(20)Z]-pregna-5,17(20)-dien-21-oyl amides were inactive.     

Pyrrolidinone-bearing methylated and halogenated benzenesulfonamides as inhibitors of carbonic anhydrases

Two series of benzenesulfonamides bearing methyl groups at ortho/ortho or meta/ortho positions and a pyrrolidinone moiety at para position were synthesized and tested as inhibitors of the twelve catalytically active human carbonic anhydrase (CA) isoforms. Observed binding affinities were determined by fluorescent thermal shift assay and intrinsic binding affinities representing the binding of benzenesulfonamide anion to the Zn(II)-bound water form of CA were calculated. Introduction of dimethyl groups into benzenesulfonamide ring decreased the binding affinity to almost all CA isoforms, but gained in selectivity towards one CA isoform. A chloro group at the meta position of 2,6-dimethylbenzenesulfonamide derivatives did not influence the binding to CA I, but it increased the affinity to all other CAs, especially, CA VII and CA XIII (up to 500 fold). The compounds may be used for further development of CA inhibitors with higher selectivity to particular CA isoforms.     

Rapid translocation and insertion of the epithelial Na+ channel in response to RhoA signaling

Activity of the epithelial Na+ channel (ENaC) is limiting for Na+ absorption across many epithelia. Consequently, ENaC is a central effector impacting systemic blood volume and pressure. Two members of the Ras superfamily of small GTPases, K-Ras and RhoA, activate ENaC. K-Ras activates ENaC via a signaling pathway involving phosphatidylinositol 3-kinase and production of phosphatidylinositol 3,4,5-trisphosphate with the phospholipid directly interacting with the channel to increase open probability. How RhoA increases ENaC activity is less clear. Here we report that RhoA and K-Ras activate ENaC through independent signaling pathways and final mechanisms of action. Activation of RhoA signaling rapidly increases the membrane levels of ENaC likely by promoting channel insertion. This process dramatically increases functional ENaC current, resulting in tight spatial-temporal control of these channels. RhoA signals to ENaC via a transduction pathway, including the downstream effectors Rho kinase and phosphatidylinositol-4-phosphate 5-kinase. Phosphatidylinositol 4,5-biphosphate produced by activated phosphatidylinositol 4-phosphate 5-kinase may play a role in targeting vesicles containing ENaC to the plasma membrane.     

Oxidative modification of M-type K(+) channels as a mechanism of cytoprotective neuronal silencing

Voltage-gated K(+) channels of the Kv7 family underlie the neuronal M current that regulates action potential firing. Suppression of M current increases excitability and its enhancement can silence neurons. We here show that three of five Kv7 channels undergo strong enhancement of their activity by oxidative modification induced by physiological concentrations of hydrogen peroxide. A triple cysteine pocket in the channel S2-S3 linker is critical for this effect. Oxidation-induced enhancement of M current produced a hyperpolarization and a dramatic reduction of action potential firing frequency in rat sympathetic neurons. As hydrogen peroxide is robustly produced during hypoxia-induced oxidative stress, we used an oxygen/glucose deprivation neurodegeneration model that showed neuronal death to be severely accelerated by M current blockade. Such blockade had no effect on survival of normoxic neurons. This work describes a novel pathway of M-channel regulation and suggests a role for M channels in protective neuronal silencing during oxidative stress.