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1%). Pb inhibited the dehydrogenase activity (DHA) by 76%, fluorescein diacetate (FDA) hydrolysis by 60%, and β-glucosidase activity by 20%. However, applied Pb increased the population of actinomycetes by 3.21 times, but significantly decreased heterotrophic bacteria by 3.40 times and N2 fixers by over 53% over control. In the second experiment, the plant was exposed to very high Pb (0, 1000, 1500, 2000, 2500, and 3000 mg kg -1) to determine the concentration up to which the plant will survive. The investigation revealed that plants could survive up to Pb 3000 mg kg-1. It confirmed the first experiment in the tolerance index, grade of growth inhibition, bioconcentration factor, translocation factor, and partitioning of Pb. Therefore, it was concluded that the cotton plant was an excluder of Pb and could be effectively cultivated for the phytostabilization of soils polluted with Pb.The health risks of polybrominated diphenyl ethers (PBDEs) to toddlers, children, and adults in creches, nursery schools, cars, and offices in Nsukka, Nigeria, via inhalation, ingestion, and dermal exposure pathways were evaluated. Eight PBDEs congeners (BDE-28, BDE-47, BDE-100, BDE-99, BDE-154, BDE-153, BDE-183, and BDE-209) were determined using gas chromatography-mass spectrometry. This is the first study on PBDEs in creches and nursery schools in Africa. Selleckchem GSK J1 The mean (median) ∑8PBDEs (ng/g) in creches, nursery schools, offices, and cars were 4355 (1850), 2095 (1130), and 37741 (2620) respectively. The concentrations of PBDEs between the three microenvironments were significantly different (p ˂ 0.05), and the highest concentration was found in cars. Ingestion of dust was the predominant pathway of exposure to PBDEs for toddlers and children, while dermal absorption was the dominant pathway for adults. Dermal absorption and ingestion in cars, creches, and nursery schools were of the same magnitude. Toddlers with the highest ingestion rate of PBDEs in creches, nursery schools, and cars are at risk especially from prolonged exposure.The dosage of contrast agents for computed tomography contrast studies is calculated based on the parameter of actual body weight (ABW) to ensure reproducibility. The use of lean body weight (LBW) and adjustment for physique (lean or obese) improves accuracy. However, this method is complex, because LBW is not a general body parameter and requires a special device to measure. To solve this problem, contrast body weight (CBW), has been proposed as a new and simple parameter that considers physique. CBW is calculated by determining the blood volume ratio based on body height, ABW, and sex and can potentially correct for body size. It can be calculated by entering a formula in a Microsoft Excel sheet. Since CBW can be easily obtained using this general tool, we decided to compare the two body parameters of ABW and CBW. We compared ABW and CBW and demonstrated a higher correlation between CBW-based dosing and the amount of iodine used per body weight than with ABW-based dosing. CBW-based dosing allows correction for body size. This indicates that contrast enhancement over a spectrum of lean or obese examinees can be linearly evaluated. To date, this method has shown good results.Melanoma is an aggressive and highly metastatic type of skin cancer where the design of new therapies is of utmost importance for the clinical management of the disease. Thus, we have aimed to investigate the mode of action by which a novel methylated analogue of L-Mimosine (e.g., L-SK-4) exerts its therapeutic potency in an in vitro model of malignant melanoma. Cytotoxicity was assessed by the Alamar Blue assay, oxidative stress by commercially available kits, ROS generation, caspase 3/7 activation and mitochondrial membrane depolarisation by flow cytometry, expression of apoptosis-related proteins by western immunoblotting and profiling of lipid biosynthesis by a metabolomic approach. Overall, higher levels of ROS, sphingolipids and apoptosis were induced by L-SK-4 suggesting that the compound's therapeutic potency is mediated through elevated ROS levels which promote the upregulation of sphingolipid (ceramide) biosynthesis thus leading to the activation of both extrinsic and intrinsic apoptosis, in an experimental model of malignant melanoma.Background Tumor-associated macrophages (TAMs) promote tumor growth, metastasis, and therapeutic resistance via colony-stimulating factor-1 (CSF-1), acting through CSF-1 receptor (CSF-1R) signaling. This phase 1 study determined the safety, tolerability, pharmacokinetics-pharmacodynamics, immunogenicity, and efficacy of the anti-CSF-1R antibody LY3022855 in solid tumors. Methods Patients with advanced solid tumors refractory to standard therapy were enrolled and treated in 2 dosing cohorts weight-based (part A) and non-weight-based (part B). Part A patients were assigned to intravenous (IV) dose-escalation cohorts 2.5 mg/kg once per week (QW), 0.3 mg/kg QW, 0.6 mg/kg QW, 1.25 mg/kg once every 2 weeks (Q2W) and 1.25 mg/kg QW doses of LY3022855. Non-weight-based doses in part B were 100 mg and 150 mg IV QW. Results Fifty-two patients (mean age 58.6 ± 10.4 years) were treated with ≥1 dose of LY3022855 (range 4-6). Five dose-limiting toxicities (left ventricular dysfunction, anemia, pancreatitis, rhabdomyolysis, and acute kidney injury) occurred in 4 patients. The non-weight-based 100 mg QW dose was established as the RP2D. The most common treatment-emergent adverse events were increase in liver function variables, fatigue, nausea, vomiting, diarrhea, anorexia, pyrexia, increased lipase, amylase, and lactate dehydrogenase. Clearance decreased with increasing dose and weight-based dosing had minimal effect on pharmacokinetics. Serum CSF-1, and IL-34 levels increased at higher doses and more frequent dosing, whereas TAMs and CD14dimCD16bright levels decreased. Three patients achieved stable disease. No responses were seen. Conclusions LY3022855 was well tolerated and showed dose-dependent pharmacokinetics-pharmacodynamics and limited clinical activity in a heterogenous solid tumor population. ClinicalTrials.gov ID NCT01346358 (Registration Date May 3, 2011).