An in situ ATR-FTIR study of mixed collectors BHA/DDA adsorption in ilmenite-titanaugite flotation system

This paper researched the enhanced flotation separation performance of ilmenite and titanaugite using the mixed collector benzhydroxamic acid/dodecylamine(BHA/DDA).The interface assembly mechanism was mainly investigated through in situ attenuated total reflectance Fourier transform infrared(ATRFTIR)spectroscopy combined with the two-dimensional correlation spectroscopy(2D-COS)and X-ray photoelectron spectroscopy(XPS).It has been found that BHA/DDA mixed collectors successfully separate ilmenite from titanaugite at a molar ratio of 8:1.Zeta potential experiments suggested that,in the presence of mixed collector system,the BHA-DDA complex adsorbed on the ilmenite surface via the chemically adsorbed BHA and the electrostatically adsorbed DDA,however,the complex adsorbed on the surface of titanaugite unstably.According to in situ ATR-FTIR combined with 2D-COS and XPS results,the interface assembly mechanism of BHA/DDA is summarized as:the function group of BHA molecules first binds to the metal sites on minerals to form bidentate ligand,then DDA co-adsorbed with BHA on the surface of minerals through hydrogen bonding.DDA may change the adsorption modes of some BHA on the ilmenite surface from four-membered ring to five-membered ring,while the modes on the titanaugite surface is true opposite.Finally,recommended adsorption configurations of the BHA/DDA complex on the two mineral surfaces are proposed.

A Case Report of MODY_(3)Combined with Intestinal Neuroendocrine Tumor

Maturity-onset diabetes of the young 3(MODY_(3))is an autosomal dominant monogenic diabetes mellitus characterized by defective p-cell function and non-insulin-dependent early-onset diabetes mellitus.The facts that patients with MODY_(3) are often misdiagnosed as type 1 and type 2 diabetes mellitus and genetic diagnosis is expensive,make its diagnosis very challenging.In this study,we reported a case of MODY_(3),which was verified to be caused by a mutation in hepatocyte nuclear factor 1αgene(c.598C>X p.Arg200Trp).In addition,the patient had a neuroendocrine tumor simultaneously,and a KMT2D gene mutation(c.5587C>G,p.Prol863Ala)might be associated with this leson.

3D anchoring structured for LiFe_(0.5)Mn_(0.5)PO_(4)@cornstalk-C cathode materials

The organic carbon source coating LiFe_(x)Mn_(1-x)PO_(4)suffers from the problem of non-uniform carbon cladding.Too thick carbon cladding layer instead hinders the de-embedding of lithium ions.In this paper,we choose cornstalk as the carbon source,then LiFe_(0.5)Mn_(0.5)PO_(4)@cornstalk-C(LFMP@C-C)with 3D anchoring structure is prepared by the solvothermal method.The results show that the LFMP with cornstalk as the carbon source has better performance compared to the sucrose-coated LFMP material(LFMP@C).The discharge capacity of LFMP@C-C is 116 mAh/g for the first cycle at 1 C and the capacity retention rate is 94.0%after 500 cycles,and the discharge capacity of LFMP@C-C is more than 17.17%higher than that of LFMP@C.

miR-137 inhibits melanoma cell proliferation through downregulation of GLO1

Late-stage melanoma is refractory to current therapies. MicroRNAs (miRNAs) can modulate many physiological and pathological processes of melanoma. Studies have demonstrated that miR-137 acts as a tumor suppressor by inhibiting the proliferation of melanoma cells through targeting multiple mRNAs. The glyoxalase system member glyoxalase 1 (GLO1) is the principal scavenging enzyme of methylglyoxal (MG), a toxic byproduct of glycolysis. Using 35S in vivo/vitro labelling analysis for dynamic proteomics (SiLAD), we found that miR-137 downregulated the expression of GLO1 in melanoma cells.Bioinformatics analysis predicted that GLO1 is a direct target of miR-137. This was validated by dual luciferase reporter assay.Quantitative RT-PCR (qRT-PCR) and western blot analysis indicated that miR-137 could decrease endogenous GLO1 expression.Furthermore, siRNA targeting of GLO1 mimicked inhibition of melanoma cell proliferation caused by miR-137 overexpression.Re-expression of GLO1 was able to restore miR-137-mediated suppression of melanoma cell proliferation. Therefore, these results suggest that miR-137 inhibits the proliferation of melanoma cells by targeting GLO1.