A Robust Recovery of Ni From Laterite Ore Promoted by Sodium Thiosulfate Through Hydrogen-Thermal Reduction.
Ontology highlight
ABSTRACT:
SUBMITTER: Liu S
PROVIDER: S-EPMC8267239 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Sodium thiosulfate (STS), first-line treatment for calcific uremic arteriolopathy, causes a mild asymptomatic acidosis in many patients. However, severe, life-threatening acidosis out of proportion with the expected acid load of STS may occur, potentially due to metabolism of STS to hydrogen sulfide.
| S-EPMC6099024 | biostudies-literature
Project description:Therapies to accelerate vascular repair are currently lacking. Pre-clinical studies suggest that hydrogen sulfide (H2S), an endogenous gasotransmitter, promotes angiogenesis. Here, we hypothesized that sodium thiosulfate (STS), a clinically relevant source of H2S, would stimulate angiogenesis and vascular repair. STS stimulated neovascularization in WT and LDLR receptor knockout mice following hindlimb ischemia as evidenced by increased leg perfusion assessed by laser Doppler imaging, and capillary density in the gastrocnemius muscle. STS also promoted VEGF-dependent angiogenesis in matrigel plugs in vivo and in the chorioallantoic membrane of chick embryos. In vitro, STS and NaHS stimulated human umbilical vein endothelial cell (HUVEC) migration and proliferation. Seahorse experiments further revealed that STS inhibited mitochondrial respiration and promoted glycolysis in HUVEC. The effect of STS on migration and proliferation was glycolysis-dependent. STS probably acts through metabolic reprogramming of endothelial cells toward a more proliferative glycolytic state. These findings may hold broad clinical implications for patients suffering from vascular occlusive diseases.
| S-EPMC9575962 | biostudies-literature
Project description:Hydrogen production from dry reforming of methane (DRM)
| S-EPMC10286284 | biostudies-literature
Project description:Background and objectiveCalcific uremic arteriolopathy (CUA) is an often fatal condition with no effective treatment. Multiple case reports and case series have described intravenous sodium thiosulfate (STS) administration in CUA, but no studies have systematically evaluated this treatment.Design, setting, participants, & measurementsThis study included 172 patients undergoing maintenance hemodialysis who had CUA and were treated with STS between August 2006 and June 2009 at Fresenius Medical Care North America. Of these, 85% completed STS therapy. Clinical, laboratory, and mortality data were abstracted from clinical information systems. Responses to survey questionnaires sent to treating physicians regarding patient-level outcomes were available for 53 patients. Effect on CUA lesions and mortality were summarized as CUA outcomes. Relevant laboratory measures, weight (using pairwise comparisons of values before, during, and after STS), and adverse events were summarized as safety parameters.ResultsMean age of the cohort was 55 years, and 74% of patients were women. Median STS dose was 25 g, and median number of doses was 38. Among surveyed patients, CUA completely resolved in 26.4%, markedly improved in 18.9%, improved in 28.3%, and did not improve in 5.7%; in the remaining patients (20.8%), the response was unknown. One-year mortality in patients treated with STS was 35%. Adverse events, laboratory abnormalities, and weight-related changes were mild. Significant reductions in serum phosphorous (P=0.02) and parathyroid hormone (P=0.01) were noted during STS treatment in patients who completed the therapy.ConclusionsAlthough conclusive evidence regarding its efficacy is lacking, a majority of patients who received STS demonstrated clinical improvement in this study.
| S-EPMC3700696 | biostudies-literature
Project description:We investigated the efficacy of sodium thiosulfate (STS) in treating hyperglycemia-induced pronephros damage in zebrafish to gain insights into the underlying mechanisms. Our results demonstrate that STS treatment effectively restored pronephros damage induced by hyperglycemia. Hyperglycemia was induced in zebrafish by suppressing the pdx1 transcription factor, which plays a crucial role in maintaining physiological pancreatic function. The pronephros structure was analyzed at 48 hours post-fertilization (hpf). Metabolomic profiling and RNA sequencing were conducted on groups subjected to various STS concentrations. Our findings reveal a downregulation of nitric oxide (NO) signaling in zebrafish with a knocked-down pdx1 gene, both metabolomically and transcriptionally. Notably, treatment with STS led to a compensatory upregulation of NO signaling, as evidenced by preliminary metabolomic data, ultimately resulting in the rescue of the pronephros structure.
2024-09-13 | GSE272119 | GEO
Project description:In order to obtain a global view of energy metabolism pathways of the sulfate-reducer Desulfovibrio vulgaris Hildenborough and the proteins involved therein whole-genome microarrays were used to compare the transcriptional response of cells grown with hydrogen/sulfate, pyruvate/sulfate, lactate/thiosulfate, and pyruvate with limiting sulfate, relative to growth in standard lactate/sulfate condition. Growth with hydrogen/sulfate showed the largest number of differently expressed genes and the largest changes in expression levels. The most up-regulated energy metabolism genes were those coding for the periplasmic [NiFeSe] hydrogenase, followed by the Ech hydrogenase, and the most down-regulated were genes coding for the Coo hydrogenase. The results point to the involvement of formate cycling and the ethanol pathway during growth on hydrogen, whereas there is evidence for CO cycling during growth on lactate and pyruvate, but not on H2. Growth with thiosulfate showed the hallmarks of a reduced energy status of the cells with down regulation of the ATP synthase and the Qmo and Dsr complexes., whereas growth with pyruvate showed the smallest differences but an increased role for the Ech hydrogenase.that in this case functions in reverse from the case of growth with H2. The multiple periplasmic hydrogenases and formate dehydrogenases, do not display the same regulation pattern showing that their metabolic roles are not totally interchangeable. This result together with the observation that several genes coding for proteins that have not been biochemically characterised were considerably affected in this study, reveals a more complex energy metabolism than previously considered and provides guidance for further studies. Keywords: Growth protocol
2008-05-31 | GSE8072 | GEO
Project description:In order to obtain a global view of energy metabolism pathways of the sulfate-reducer Desulfovibrio vulgaris Hildenborough and the proteins involved therein whole-genome microarrays were used to compare the transcriptional response of cells grown with hydrogen/sulfate, pyruvate/sulfate, lactate/thiosulfate, and pyruvate with limiting sulfate, relative to growth in standard lactate/sulfate condition. Growth with hydrogen/sulfate showed the largest number of differently expressed genes and the largest changes in expression levels. The most up-regulated energy metabolism genes were those coding for the periplasmic [NiFeSe] hydrogenase, followed by the Ech hydrogenase, and the most down-regulated were genes coding for the Coo hydrogenase. The results point to the involvement of formate cycling and the ethanol pathway during growth on hydrogen, whereas there is evidence for CO cycling during growth on lactate and pyruvate, but not on H2. Growth with thiosulfate showed the hallmarks of a reduced energy status of the cells with down regulation of the ATP synthase and the Qmo and Dsr complexes., whereas growth with pyruvate showed the smallest differences but an increased role for the Ech hydrogenase.that in this case functions in reverse from the case of growth with H2. The multiple periplasmic hydrogenases and formate dehydrogenases, do not display the same regulation pattern showing that their metabolic roles are not totally interchangeable. This result together with the observation that several genes coding for proteins that have not been biochemically characterised were considerably affected in this study, reveals a more complex energy metabolism than previously considered and provides guidance for further studies. Keywords: Growth protocol Desulfovibrio vulgaris Hildenborough was cultured at 37°C with thiosulfate as the only electron acceptor (with lactate as the electron donor) to mid-log phase. Cultures were also cultivated similarly using sulfate as the sole electron acceptor to mid-log phase. Gene expression profiles of cultures grown with thiosulfate as the electron acceptor were compared with those of the cultures grown with sulfate as the electron acceptor for dissimilatory sulfate reductiontion. Total RNA was harvested from four replicate cultures for microarray analysis. RNA extraction, purification, and labeling were performed independently on each cell sample. Two samples of each total RNA preparation were labeled, one with Cy3-dUTP and another with Cy5-dUTP for microarray hybridization (dye swap).
2008-05-31 | E-GEOD-8072 | biostudies-arrayexpress
Project description:Increasing nickel (Ni) demand may spur the need for creative Ni production methods. Agromining (farming for metals) uses plants that can accumulate high concentrations of metal in their biomass, called bio-ore, as a metal extraction strategy. Furthermore, biochar, produced by biomass pyrolysis under low-oxygen conditions, can be used to remove Ni from contaminated wastewaters. In this work we investigate whether biochar synthesized from the Ni-hyperaccumulating plant Odontarrhena chalcidica (synonymous Alyssum murale) can be used as a Ni-adsorbing biochar. We grew O. chalcidica on soils with varying Ni concentration, characterized the plants and resultant biochars synthesized at different pyrolysis temperatures, and analyzed Ni batch adsorption results to determine the adsorption capacity of O. chalcidica biochar. We found that Ni concentration in O. chalcidica increases with increasing soil Ni but reaches an accumulation limit around 23 g Ni kg-1 dry weight in dried leaf samples. Pyrolysis concentrated Ni in the biochar; higher pyrolysis temperatures led to higher biochar Ni concentrations (max. 87 g Ni kg-1) and surface areas (max. 103 m2/g). Finally, the O. chalcidica biochar adsorption results were comparable to high-performing Ni adsorbents in the literature. The adsorption process greatly increased the Ni concentration in some biochars, indicating that synthesizing biochar from O. chalcidica biomass and using it as a Ni adsorbent can produce a Ni-enhanced bio-ore with nickel content higher than all nickel-rich veins currently mined.
| S-EPMC8778606 | biostudies-literature
Project description:BackgroundCisplatin chemotherapy and surgery are effective treatments for children with standard-risk hepatoblastoma but may cause considerable and irreversible hearing loss. This trial compared cisplatin with cisplatin plus delayed administration of sodium thiosulfate, aiming to reduce the incidence and severity of cisplatin-related ototoxic effects without jeopardizing overall and event-free survival.MethodsWe randomly assigned children older than 1 month and younger than 18 years of age who had standard-risk hepatoblastoma (≤3 involved liver sectors, no metastatic disease, and an alpha-fetoprotein level of >100 ng per milliliter) to receive cisplatin alone (at a dose of 80 mg per square meter of body-surface area, administered over a period of 6 hours) or cisplatin plus sodium thiosulfate (at a dose of 20 g per square meter, administered intravenously over a 15-minute period, 6 hours after the discontinuation of cisplatin) for four preoperative and two postoperative courses. The primary end point was the absolute hearing threshold, as measured by pure-tone audiometry, at a minimum age of 3.5 years. Hearing loss was assessed according to the Brock grade (on a scale from 0 to 4, with higher grades indicating greater hearing loss). The main secondary end points were overall survival and event-free survival at 3 years.ResultsA total of 109 children were randomly assigned to receive cisplatin plus sodium thiosulfate (57 children) or cisplatin alone (52) and could be evaluated. Sodium thiosulfate was associated with few high-grade toxic effects. The absolute hearing threshold was assessed in 101 children. Hearing loss of grade 1 or higher occurred in 18 of 55 children (33%) in the cisplatin-sodium thiosulfate group, as compared with 29 of 46 (63%) in the cisplatin-alone group, indicating a 48% lower incidence of hearing loss in the cisplatin-sodium thiosulfate group (relative risk, 0.52; 95% confidence interval [CI], 0.33 to 0.81; P=0.002). At a median of 52 months of follow-up, the 3-year rates of event-free survival were 82% (95% CI, 69 to 90) in the cisplatin-sodium thiosulfate group and 79% (95% CI, 65 to 88) in the cisplatin-alone group, and the 3-year rates of overall survival were 98% (95% CI, 88 to 100) and 92% (95% CI, 81 to 97), respectively.ConclusionsThe addition of sodium thiosulfate, administered 6 hours after cisplatin chemotherapy, resulted in a lower incidence of cisplatin-induced hearing loss among children with standard-risk hepatoblastoma, without jeopardizing overall or event-free survival. (Funded by Cancer Research UK and others; SIOPEL 6 ClinicalTrials.gov number, NCT00652132 ; EudraCT number, 2007-002402-21 .).
| S-EPMC6117111 | biostudies-literature
Project description:In this proof-of-principle trial, the hypothesis was investigated that sodium thiosulfate (STS), a potent antioxidant and hydrogen sulfide donor, reduces reperfusion injury. A total of 373 patients presenting with a first ST-segment elevation myocardial infarction received either 12.5 g STS intravenously or matching placebo at arrival at the hospital and 6 hours later. The primary outcome, infarct size, measured by cardiac magnetic resonance at 4 months after randomization, did not differ between the treatment arms. Secondary outcomes were comparable as well, suggesting no clinical benefit of STS in this population at relatively low risk for large infarction.
| S-EPMC10714171 | biostudies-literature