Biodegradation Assessment of Petroleum-Contaminated Soils by Natural Attenuation, Biostimulation and Bioaugmentation Methods on an Industrial Scale

This research study compares the biodegradation of petroleum hydrocarbons by natural attenuation, biostimulation and bioaugmentation methods by applying the Pseudomonas aeruginosa and Bacillus cereus bacteria in hydrocarbon-polluted land area of 1000 square meters consists of three distinct parts to compare the methods discussed above for 100 days. The petroleum-contaminated percentage of this area (w / w) is 0.5%. The extraction and determination of petroleum hydrocarbons percentage in contaminated soil was done by gravimetric method by liquid-liquid extraction method by hexane, dichloromethane and chloroform solvents. The results showed that the bioaugmentation technique has a higher ability to analyze the petroleum hydrocarbons contaminant that reduced about 82.33% of this pollution in the period of 100 days and biostimulation and natural attenuation methods decreased the hydrocarbon materials percentage to the rate of 40.32 and 12.11% respectively

Biodegradation Assessment of Petroleum-Contaminated Soils by Natural Attenuation, Biostimulation and Bioaugmentation Methods on an Industrial Scale

This research study compares the biodegradation of petroleum hydrocarbons by natural attenuation, biostimulation and bioaugmentation methods by applying the Pseudomonas aeruginosa and Bacillus cereus bacteria in hydrocarbon-polluted land area of 1000 square meters consists of three distinct parts to compare the methods discussed above for 100 days. The petroleum-contaminated percentage of this area (w / w) is 0.5%. The extraction and determination of petroleum hydrocarbons percentage in contaminated soil was done by gravimetric method by liquid-liquid extraction method by hexane, dichloromethane and chloroform solvents. The results showed that the bioaugmentation technique has a higher ability to analyze the petroleum hydrocarbons contaminant that reduced about 82.33% of this pollution in the period of 100 days and biostimulation and natural attenuation methods decreased the hydrocarbon materials percentage to the rate of 40.32 and 12.11% respectively

TMEM97 and PGRMC1 do not mediate sigma-2 ligand-induced cell death

Abstract Sigma-2 receptors have been implicated in both tumor proliferation and neurodegenerative diseases. Recently the sigma-2 receptor was identified as transmembrane protein 97 (TMEM97). Progesterone receptor membrane component 1 (PGRMC1) was also recently reported to form a complex with TMEM97 and the low density lipoprotein (LDL) receptor, and this trimeric complex is responsible for the rapid internalization of LDL. Sigma-2 receptor ligands with various structures have been shown to induce cell death in cancer cells. In the current study, we examined the role of TMEM97 and PGRMC1 in mediating sigma-2 ligand-induced cell death. Cell viability and caspase-3 assays were performed in control, TMEM97 knockout (KO), PGRMC1 KO, and TMEM97/PGRMC1 double KO cell lines treated with several sigma-2 ligands. The data showed that knockout of TMEM97, PGRMC1, or both did not affect the concentrations of sigma-2 ligands that induced 50% of cell death (EC50), suggesting that cytotoxic effects of these compounds are not mediated by TMEM97 or PGRMC1. Sigma-1 receptor ligands, (+)-pentazocine and NE-100, did not block sigma-2 ligand cytotoxicity, suggesting that sigma-1 receptor was not responsible for sigma-2 ligand cytotoxicity. We also examined whether the alternative, residual binding site (RBS) of 1,3-Di-o-tolylguanidine (DTG) could be responsible for sigma-2 ligand cytotoxicity. Our data showed that the binding affinities (K i) of sigma-2 ligands on the DTG RBS did not correlate with the cytotoxicity potency (EC50) of these ligands, suggesting that the DTG RBS was not fully responsible for sigma-2 ligand cytotoxicity. In addition, we showed that knocking out TMEM97, PGRMC1, or both reduced the initial internalization rate of a sigma-2 fluorescent ligand, SW120. However, concentrations of internalized SW120 became identical later in the control and knockout cells. These data suggest that the initial internalization process of sigma-2 ligands does not appear to mediate the cell-killing effect of sigma-2 ligands. In summary, we have provided evidence that sigma-2 receptor/TMEM97 and PGRMC1 do not mediate sigma-2 ligand cytotoxicity. Our work will facilitate elucidating mechanisms of sigma-2 ligand cytotoxicity

Rapid Cu-Catalyzed [²¹¹At]Astatination and [¹²⁵I]Iodination of Boronic Esters at Room Temperature

Access to ²¹¹At- and ¹²⁵I-radiolabeled compounds in excellent RCCs and RCYs was achieved in just 10 min at room temperature using a Cu catalyst. The reaction conditions are applicable to a broad class of aryl and heteroaryl boronic reagents with varying steric and electronic properties as well as late-stage astatination and iodination of anticancer PARP inhibitors. This protocol eliminates the traditional need for toxic organotin reagents, elevated temperatures, and extended reaction times, providing a more practical and environmentally friendly approach to developing α-emitting radiotherapeutics

Improved safety and efficacy of 213Bi-DOTATATE-targeted alpha therapy of somatostatin receptor-expressing neuroendocrine tumors in mice pre-treated with l-lysine

textabstractBackground: Targeted alpha therapy (TAT) offers advantages over current β-emitting conjugates for peptide receptor radionuclide therapy (PRRT) of neuroendocrine tumors. PRRT with 177Lu-DOTATATE or 90Y-DOTATOC has shown dose-limiting nephrotoxicity due to radiopeptide retention in the proximal tubules. Pharmacological protection can reduce renal uptake of radiopeptides, e.g., positively charged amino acids, to saturate in the proximal tubules, thereby enabling higher radioactivity to be safely administered. The aim of this preclinical study was to evaluate the therapeutic effect of 213Bi-DOTATATE with and without renal protection using L-lysine in mice. Tumor uptake and kinetics as a function of injected mass of peptide (range 0.03–3 nmol) were investigated using 111In-DOTATATE. These results allowed estimation of the mean radiation absorbed tumor dose for 213Bi-DOTATATE. Pharmacokinetics and dosimetry of 213Bi-DOTATATE was determined in mice, in combination with renal protection. A dose escalation study with 213Bi-DOTATATE was performed to determine the maximum tolerated dose (MTD) with and without pre-administration of l-lysine as for renal protection. Neutrophil gelatinase-associated lipocalin (NGAL) served as renal biomarker to determine kidney injury. Results: The maximum mean radiation absorbed tumor dose occurred at 0.03 nmol and the minimum at 3 nmol. Similar mean radiation absorbed tumor doses were determined for 0.1 and 0.3 nmol with a mean radiation absorbed dose of approximately 0.5 Gy/MBq 213Bi-DOTATATE. The optimal mass of injected peptide was found to be 0.3 nmol. Tumor uptake was similar for 111In-DOTATATE and 213Bi-DOTATATE at 0.3 nmol peptide. Lysine reduced the renal uptake of 213Bi-DOTATATE by 50% with no effect on the tumor uptake. The MTD was <13.0 ± 1.6 MBq in absence of l-lysine and 21.7 ± 1.9 MBq with l-lysine renal protection, both imparting an LD50 mean renal radiation absorbed dose of 20 Gy. A correlation was found between the amount of injected radioactivity and NGAL levels. Conclusions: The therapeutic potential of 213Bi-DOTATATE was illustrated by significantly decreased tumor burden and improved overall survival. Renal protection with l-lysine immediately prior to TAT with 213Bi-DOTATATE prolonged survival providing substantial evidence for pharmacological nephron blockade to mitigate nephrotoxicity