In this work a Chemical treatment process by sulphuric Acid leaching has been carried out for the dephosphorization of Wadi Alshatti iron ore, which contains an average of 0.87% of phosphorus content. Sulphuric acid is used for the preparation of leaching solutions. This study involves The effects of leaching concentration, acid : ore ratio, contact time, leaching temperature and partical size on the dephosphorization of wadi Alshatti iron ore by chemical leaching [H₂SO₄] technique in a batch mode, the results indicates that 90.8% of phosphorus is removed (0.08%) at 30 min leaching time, 0.3M leachant concentration, 2:1 acid : ore ratio, 60 ⁰C leaching temperature and 80µm partical size which were the optimum conditions for the removal of P from wadi Alshatti iron ore. Iron loss during the leaching was less than 2%.

It can be concluded that acid leaching of Wadi Alshatti iron ore is feasible using the conditions of the described process.

Key words: iron ore, chemical treatment, dephosphorization, sulphuric acid, phosphorus.

Abstract

Background: Under inflammatory conditions, the activation of corticotropin-releasing factor (CRF) receptor has been shown to inhibit pain through opioid peptide release from immune cells or neurons. CRF's effects on human and animal pain modulation depend, however, on the distribution of its receptor subtypes 1 and 2 (CRF-R1 and CRF-R2) along the neuraxis of pain transmission. The objective of this study is to investigate the respective role of each CRF receptor subtype on centrally administered CRF-induced antinociception during inflammatory pain.

Methods: The present study investigated the role of intracerebroventricular (i.c.v.) CRF receptor agonists on nociception and the contribution of cerebral CRF-R1 and/or CRF-R2 subtypes in an animal model of Freund's complete adjuvant (FCA)-induced hind paw inflammation. Methods used included behavioral experiments, immunofluorescence confocal analysis, and reverse transcriptase-polymerase chain reaction.

Results: Intracerebroventricular, but systemically inactive, doses of CRF elicited potent, dose-dependent antinociceptive effects in inflammatory pain which were significantly antagonized by i.c.v. CRF-R1-selective antagonist NBI 27914 (by approximately 60%) but less by CRF-R2-selective antagonist K41498 (by only 20%). In line with these findings, i.c.v. administration of CRF-R1 agonist stressin I produced superior control of inflammatory pain over CRF-R2 agonist urocortin-2. Intriguingly, i.c.v. opioid antagonist naloxone significantly reversed the CRF as well as CRF-R1 agonist-elicited pain inhibition. Consistent with existing evidence of high CRF concentrations in brain areas such as the thalamus, hypothalamus, locus coeruleus, and periaqueductal gray following its i.c.v. administration, double-immunofluorescence confocal microscopy demonstrated primarily CRF-R1-positive neurons that expressed opioid peptides in these pain-relevant brain areas. Finally, PCR analysis confirmed the predominant expression of the CRF-R1 over CRF-R2 in representative brain areas such as the hypothalamus.

Conclusion: Taken together, these findings suggest that CRF-R1 in opioid-peptide-containing brain areas plays an important role in the modulation of inflammatory pain and may be a useful therapeutic target for inflammatory pain control.