Investigation of the enrichment-purification process and electrochemical performance of kish graphite in dust from blast furnace tapping yard.

Kish graphite is a typical byproduct of steel production, and its enrichment and purification are essential prerequisites for its high value and comprehensive utilization. To solve the problem of recovery and application of difficult-to-treat kish graphite with a small particle size obtained from metallurgical dust, kish graphite in blast furnace tapping yard dust was effectively enriched and purified by a comprehensive flotation-acid leaching treatment process in this study. The influence of the flotation agents on the flotation process was explored. The results showed that the optimized flotation agent dosage was 500.0 g·t-1 (collector) and 120.0 g·t-1 (frother), respectively. Based on the optimized flotation scheme, a graphite concentrate (FG) with 79.12 % carbon content and 93.5 % carbon recovery was obtained. After the leaching treatment with a HCl-HF mixed acid solution, the carbon content of the graphite concentrate increased to 95.55 %. The ID/IG value of the graphite concentrate was 0.145, and the average lattice spacing was approximately 0.3354 nm. The SEM results showed that the leaching-treated graphite concentrate (AFG) had a loose, fragment-like structure. When used as an anode material for lithium-ion batteries, The AFG still provided a high reversible capacity of âˆ¼370 mAh·g-1 and excellent coulombic efficiency of 99.6 % after 350 cycles. In addition, an industrial-grade recycling and utilization path for kish graphite based on a circular supply chain strategy was proposed. The results of this study may serve as a conceptual basis for the recovery and application of kish graphite from metallurgical dust.

The stability of the compounds formed in the process of removal Pb(II), Cu(II) and Cd(II) by steelmaking slag in an acidic aqueous solution.

The potential feasibility of steel slag as a low cost removal agent for heavy metal ions Pb(II), Cu(II) and Cd(II) in acidic conditions was investigated in this study. The initial pH effect on heavy metal ion removal efficiency, the compounds formed after heavy metal ion removal, and the binding force of metals with the compounds were determined. The results showed that the efficiency of removing heavy metal ions by steel slag was low at low initial pH levels, yet it sharply increased and then became stable as the initial pH increased. The pseudo-second order model provided the best description for the removal of Pb, Cu, and Cd ions, indicating that the predominant heavy metal ion removal mechanism was chemisorption. The images obtained by the Fourier transform infrared spectroscopy (FTIR) and the X-ray diffraction (XRD) analysis indicated that the main compounds formed after the removal of Pb, Cu, and Cd ions by steel slag in an aqueous solution were heavy metal ferrites, silicates, carbonates, hydroxides and oxides. Sequential extraction experiments showed that these three heavy metals bond to the compounds mainly in the carbonate fraction (F2), the Fe oxide bound fractions (F3 (a) and F3 (c)), and the residual fraction (F4) in which F2 corresponded to the carbonates, and F3(a), F3(c) and F4 corresponded to the amorphous or crystalline ferrites and silicates, respectively. The F3 (a), F3 (c) and F4 are relatively stable and do not tend to re-release metal ions in acidic solutions. However, F2 and heavy metal hydroxides have relatively low stability and dissolve readily, re-leaching heavy metal ions into the acid solution. When these three heavy metal ion mixtures were removed by steel slag, the Pb, Cu and Cd deposits were at higher levels in the F3 and F4 fractions. Therefore, it was concluded that the co-existence of heavy metal ions in an aqueous solution is beneficial for their removal by steel slag in acidic conditions.

Antinociceptive Effect of Ghrelin in a Rat Model of Irritable Bowel Syndrome Involves TRPV1/Opioid Systems.

BACKGROUND/AIMS: Irritable bowel syndrome (IBS), defined as recurrent abdominal pain and changes in bowel habits, seriously affects quality of life and ability to work. Ghrelin is a brain-gut hormone, which has been reported to show antinociceptive effects in peripheral pain. We investigated the effect of ghrelin on visceral hypersensitivity and pain in a rat model of IBS. METHODS: Maternal deprivation (MD) was used to provide a stress-induced model of IBS in Wistar rats. Colorectal distension (CRD) was used to detect visceral sensitivity, which was evaluated by abdominal withdrawal reflex (AWR) scores. Rats that were confirmed to have visceral hypersensitivity after MD were injected with ghrelin (10 µg/kg) subcutaneously twice a week from weeks 7 to 8. [D-Lys3]-GHRP-6 (100 nmol/L) and naloxone (100 nmol/L) were administered subcutaneously to block growth hormone secretagogue receptor 1α (GHS-R1α) and opioid receptors, respectively. Expression of transient receptor potential vanilloid type 1 (TRPV1) and µ and κ opioid receptors (MOR and KOR) in colon, dorsal root ganglion (DRG) and cerebral cortex tissues were detected by western blotting, quantitative real-time polymerase chain reaction (qRT-PCR), immunohistochemical analyses and immunofluorescence. RESULTS: Ghrelin treatment increased expression of opioid receptors and inhibited expression of TRPV1 in colon, dorsal root ganglion (DRG) and cerebral cortex. The antinociceptive effect of ghrelin in the rat model of IBS was partly blocked by both the ghrelin antagonist [D-Lys3]-GHRP-6 and the opioid receptor antagonist naloxone. CONCLUSION: The results indicate that ghrelin exerted an antinociceptive effect, which was mediated via TRPV1/opioid systems, in IBS-induced visceral hypersensitivity. Ghrelin might potentially be used as a new treatment for IBS.

The effect of ghrelin on cell proliferation in small intestinal IEC-6 cells.

BACKGROUND AND AIMS: Recent evidence demonstrates that ghrelin, a short orexigenic peptide from the stomach, has dual effects on cell proliferation in different cell types via autocrine and/or paracrine mechanisms. The aim of this study is to investigate the proliferative role of ghrelin in intestinal epithelial IEC-6 cells and explore underlying mechanism. METHODS: RT-PCR was used for the detection of growth hormone secretagogue receptor 1a. Cell proliferation was measured using Cell Counting Kit-8. Protein expression of ERK 1/2 and Akt was examined using western blotting. Inhibitors of mitogen activated protein kinases kinase and phosphatidylinositol 3-kinase were used to evaluate the role of these signalling pathways in ghrelin-induced proliferation of IEC-6 cells. RESULTS: Growth hormone secretagogue receptor 1a mRNA was present in IEC-6 cells. Ghrelin and des-acyl ghrelin increased IEC-6 cell proliferation in a dose- and time-dependent manner. Ghrelin and des-acyl ghrelin activated ERK1/2, but not Akt. U0126, a specific inhibitor of mitogen activated protein kinases kinase, blocked ghrelin- and des-acyl ghrelin-induced ERK1/2 phosphorylation and cell proliferation in IEC-6 cells. CONCLUSION: Ghrelin and des-acyl ghrelin stimulate the proliferation of IEC-6 cells via the ERK1/2 pathway.

[Study on the relationship between function of blood and tumor recurrence in oral squamous cell carcinomas].

OBJECTIVE: To explore the coagulation indexes and offer a valuable reference for clinic therapy and prognosis in patients with oral squamous cell carcinomas (OSCCs). METHODS: The indexes of prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT) and fibrinogen (Fib) were detected by using automatic blood coagulation testing machine in 65 healthy people and 351 patients with OSCCs. All patients with OSCCs were divided into three groups included primary tumor, neck metastasis of lymph nodes and recurrence. The data were analysed by SPSS 11.0. RESULTS: The index of PT in patients with OSCCs was longer than that of healthy people. There was a significance between the control group and the group with the neck metastasis of lymph node or the recurrence group (P<0.01). The time of APTT was shortened. Except for the group with the neck metastasis of lymph node and the recurrence group the distinctive difference existed in other groups(P<0.05). There was no significance between two groups in the indexes of TT and Fib (P>0.05). CONCLUSION: PT and APTT may be the useful indexes for clinic therapy and prognosis in patients with oral squamous cell carcinomas.

Molecule action mechanisms of NM-3 on human gastric cancer SGC-7901 cells in vivo or in vitro.

AIM: To study the molecule action mechanisms of NM-3 on the growth of human gastric cancer SGC-7901 cells in vivo or in vitro. METHODS: SGC-7901 from human non-differentiated gastric cancer cell line was cultured with NM-3 at 100 mg/ml for 24 h. We observed its inhibitory rate and the density of micro-vascular growth in grafted mice with human gastric cancer SGC-7901. The apoptosis of human gastric cancer SGC-7901 was revealed in NM-3 treatment group by using terminal deoxynucleotidyl transferase-mediated deoxy-uridine triphosphate-fluorescene nick end labeling (TUNEL) method and flow cytometry analysis. RESULTS: The growth of SGC-7901 cells was markedly inhibited compared with control growp, which was smaller than that in normal saline control group (4.17 g+/-0.22 g vs 9.45 g+/-1.38 g, P<0.01). The level of apoptosis of human gastric cell line SGC-7901 was obviously increased in NM-3 treatment group at 1 mg.L(-1) for 24 h. NM-3 inducing apoptotic index in NM-3 plus carboplatin group was 3.5 times that of carboplatin control group (TUNEL: 27.98+/-6.12% vs 12.94+/-2.12%, FACScan: 26.86+/-5.69% vs 11.86+/-1.09%, P<0.01). Western blot analysis showed that the apoptotic index of human gastric cancer was elevated for 12, 24 and 36 h with an evident time-effect relationship in groups at 100 mg.L(-1). NM-3 enhanced the inhibitive effects and sensitivity of chemotherapy for human gastric cancer in nude mice. These results suggested that NM-3 played a key inhibitive role in the growth of grafted human gastric cancer in nude mice. CONCLUSION: NM-3 can inhibit the growth of human gastric cancer cell line SGC-7901, and enhance the sensitivity of carboplatin on SGC-7901 and induced its apoptosis.