Empirical model to assess leaching of pesticides in soil under a steady-state flow and tropical conditions.

Abstract: An empirical model of leaching of pesticides was developed to simulate the concentration of fungicides throughout unsaturated soil. The model was based on chemical reactions and the travel time of a conservative tracer to represent the travel time required for water to flow between soil layers. The model's performance was then tested using experimental data from dimethomorph and pyrimethanil applied to the soil under field and laboratory conditions. The empirical model simulated fungicide concentration on soil solids and in soil solution at different depths over time (mean square error between 2.9 mg2 kg-2 and 61mg2 kg-2) using sorption percentages and degradation rates under laboratory conditions. The sorption process was affected by the organic carbon, clay, and the effective cation exchange capacity of the soil. The degradation rate values of dimethomorph (0.039 d-1-0.009 d-1) and pyrimethanil (0.053 d-1-0.004 d-1) decreased from 0 to 40 cm and then remained constant in deeper soil layers (60-80 cm). Fungicide degradation was a critical input in the model at subsurface layers. The model was determined to be a reliable mathematical tool to estimate the leachability of pesticides in tropical soil under a steady-state flow. It may be extended to other substances and soils for environmental risk assessment projects. Supplementary Information: The online version contains supplementary material available at 10.1007/s13762-023-05038-w.

Transanal endoscopic surgery with a 3D printed device.

BACKGROUND: The aim of this study was to investigate the effectiveness of devices manufactured with 3D printing for performing transanal endoscopic procedures without pneumorectum. METHODS: Functional devices were designed in the Polytechnic School of Engineering of Gijón from 2016 to 2018 using three-dimensional (3D) solid modelling software (Solid-Works®), that allows customization of the device (diameter and length). The devices were made in acrylonitrile butadiene styrene (ABS) by additive manufacturing using an HP Designjet 3D Printer, with fused deposition modelling (FDM) technology. Tests were carried out on mixed simulators (with viscera) and cadavers with a prototype in the form of an open cylindrical base ellipsoid spindle with two bars. In this paper, we present the information of the first series of patients in which this device has been used to perform a full-thikness endoscopic resection of the rectal wall without pneumorectum. The characteristics of the patients, size, and location of the lesion, the type of anesthesia used, the duration of the procedure, hospital stay, complications, and pathology were analyzed. An endoscopic follow-up was also carried out for at least 2 years. RESULTS: Seven interventions were carried out in six patients. The lesions were located at a mean distance of 5 cm from the anal verge and an average area of 11.8 cm2. Four of the procedures were performed with general anesthesia and 3 with spinal anesthesia. Histopathology examination identified 3 adenomas, 3 pT1 and 1 pT2 adenocarcinomas. All excisions were full thickness. En bloc excision was possible in all cases. In only one case of a benign polyp there was a positive lateral margin. As regards complications, there was one case of postoperative rectal bleeding without the need for transfusions. There were no readmissions and no postoperative mortality. CONCLUSIONS: An innovative device made with a 3D printer can be used successfully in transanal endoscopic resections of the rectal wall, with spinal anaesthesia and avoiding the need for pneumorectum.

Antimicrobial susceptibility and molecular typing of toxigenic clinical isolates of Clostridium difficile causing infections in the south of Spain.

Antimicrobial susceptibility to 6 antimicrobial agents, PCR-ribotyping and molecular genetics of fluoroquinolone resistance was assessed in 70 toxigenic clinical isolates of C. difficile recovered from patients attended in a hospital in southern Spain with suspected Clostridium difficile infection. Moxifloxacin was the least active drug, mainly driven by the aminoacid substitution Thr82Ile in GyrA, while PCR-ribotype 078 was the most prevalent lineage identified and grouped several of the fluoroquinolone resistant isolates.

Fas/Fas ligand regulation mediates cell death in human Ewing's sarcoma cells treated with melatonin.

BACKGROUND: Despite recent advances in cancer therapy, the 5-year survival rate for Ewing's sarcoma is still very low, and new therapeutic approaches are necessary. It was found previously that melatonin induces cell death in the Ewing's sarcoma cell line, SK-N-MC, by activating the extrinsic apoptotic pathway. METHODS: Melatonin actions were analysed by metabolic viability/survival cell assays, flow cytometry, quantitative PCR for mRNA expression, western blot for protein activation/expression and electrophoretic mobility shift assay for transcription factor activation. RESULTS: Melatonin increases the expression of Fas and its ligand Fas L, this increase being responsible for cell death induced by the indolamine. Melatonin also produces a transient increase in intracellular oxidants and activation of the redox-regulated transcription factor Nuclear factor-kappaB. Inhibition of such activation prevents cell death and Fas/Fas L upregulation. Cytotoxic effect and Fas/Fas L regulation occur in all Ewing's cell lines studied, and do not occur in the other tumour cell lines studied where melatonin does not induce cell death. CONCLUSION: Our data offers new insights in the study of alternative therapeutic strategies in the treatment of Ewing's sarcoma. Further attention deserves to be given to the differences in the cellular biology of sensitive tumours that could explain the cytotoxic effect of melatonin and the increase in the level of free radicals caused by this molecule, in particular cancer types.

Antioxidants do not prevent acrylonitrile-induced toxicity.

Several reports have recently described that acrylonitrile (ACN) toxicity resides in its capacity for inducing oxidative stress. ACN can be conjugated with glutathione (GSH), diminishing its cellular content, or being metabolized to cyanide. In the present report, we determine the effect of ACN on the viability of primary-cultured astrocytes as well as the oxidative damage generated by ACN by measuring GSH levels in primary cultured astrocytes. We also analyzed whether the ACN (2.5mM) toxicity could be avoided by using antioxidants such as taurine (5mM), N-acetylcysteine (20 mM), trolox (100 microM), estradiol (10 microM) and melatonin (100 nM-1mM). In this cell culture model, antioxidants were not able to prevent ACN-induced cell damage, with the exception of NAC, confirming that only GSH seems to play a key role in ACN-derived toxicity. Additionally, we measured different parameters of oxidative stress such as catalase activity, lipid peroxidation and GSH concentration, as indicators of the potential oxidative stress mediated by the toxicity of ACN, after exposure of Wistar rats to a concentration of 200 ppm ACN for 14 days. At the concentration assayed, we did not find any evidence of oxidative damage in the brain of ACN-treated rats.