Research Status and Development of Non-Ferrous Metal Beneficiation Wastewater Treatment

Non-ferrous metal beneficiation wastewater is often acidic or alkaline, and contains a large number of residual reagents, suspended solids and metal ions-based pollutants. With the continuous development and utilization of mineral resources, non-ferrous metal beneficiation wastewater has become a major cause of mine environment, water and soil pollution. The wastewater from mineral processing can not be applied to mineral processing. This was accounted by the fact that all kinds of pollutants can damage mineral processing equipment, affect mineral processing flowsheet and decrease concentrate quality. Therefore, the comprehensive treatment of non-ferrous metal beneficiation wastewater has become an urgent problem that needs to be solved in China and even in the world. This article summarizes the treatment methods of the main pollutants that are generated from non-ferrous metal beneficiation wastewater, expounds the current research status of non-ferrous metal beneficiation wastewater treatment in recent years, looks forward to future development direction of wastewater treatment

Effect of a low-protein diet supplemented with ketoacids on skeletal muscle atrophy and autophagy in rats with type 2 diabetic nephropathy.

A low-protein diet supplemented with ketoacids maintains nutritional status in patients with diabetic nephropathy. The activation of autophagy has been shown in the skeletal muscle of diabetic and uremic rats. This study aimed to determine whether a low-protein diet supplemented with ketoacids improves muscle atrophy and decreases the increased autophagy observed in rats with type 2 diabetic nephropathy. In this study, 24-week-old Goto-Kakizaki male rats were randomly divided into groups that received either a normal protein diet (NPD group), a low-protein diet (LPD group) or a low-protein diet supplemented with ketoacids (LPD+KA group) for 24 weeks. Age- and weight-matched Wistar rats served as control animals and received a normal protein diet (control group). We found that protein restriction attenuated proteinuria and decreased blood urea nitrogen and serum creatinine levels. Compared with the NPD and LPD groups, the LPD+KA group showed a delay in body weight loss, an attenuation in soleus muscle mass loss and a decrease of the mean cross-sectional area of soleus muscle fibers. The mRNA and protein expression of autophagy-related genes, such as Beclin-1, LC3B, Bnip3, p62 and Cathepsin L, were increased in the soleus muscle of GK rats fed with NPD compared to Wistar rats. Importantly, LPD resulted in a slight reduction in the expression of autophagy-related genes; however, these differences were not statistically significant. In addition, LPD+KA abolished the upregulation of autophagy-related gene expression. Furthermore, the activation of autophagy in the NPD and LPD groups was confirmed by the appearance of autophagosomes or autolysosomes using electron microscopy, when compared with the Control and LPD+KA groups. Our results showed that LPD+KA abolished the activation of autophagy in skeletal muscle and decreased muscle loss in rats with type 2 diabetic nephropathy

Table_1_Separating the effects of life course adiposity on diabetic nephropathy: a comprehensive multivariable Mendelian randomization study.docx

AimsPrevious Mendelian randomization (MR) of obesity and diabetic nephropathy (DN) risk used small sample sizes or focused on a single adiposity metric. We explored the independent causal connection between obesity-related factors and DN risk using the most extensive GWAS summary data available, considering the distribution of adiposity across childhood and adulthood.MethodsTo evaluate the overall effect of each obesity-related exposure on DN (Ncase = 3,676, Ncontrol = 283,456), a two-sample univariate MR (UVMR) analysis was performed. The independent causal influence of each obesity-related feature on DN was estimated using multivariable MR (MVMR) when accounting for confounding variables. It was also used to examine the independent effects of adult and pediatric obesity, adjusting for their interrelationships. We used data from genome-wide association studies, including overall general (body mass index, BMI) and abdominal obesity (waist-to-hip ratio with and without adjustment for BMI, i.e., WHR and WHRadjBMI), along with childhood obesity (childhood BMI).ResultsUVMR revealed a significant association between adult BMI (OR=1.24, 95%CI=1.03-1.49, P=2.06×10-2) and pediatric BMI (OR=1.97, 95%CI=1.59-2.45, P=8.55×10-10) with DN risk. At the same time, adult WHR showed a marginally significant increase in DN (OR =1.27, 95%CI = 1.01-1.60, P=3.80×10-2). However, the outcomes were adverse when the influence of BMI was taken out of the WHR (WHRadjBMI). After adjusting for childhood BMI, the causal effects of adult BMI and adult abdominal obesity (WHR) on DN were significantly attenuated and became nonsignificant in MVMR models. In contrast, childhood BMI had a constant and robust independent effect on DN risk(adjusted for adult BMI: IVW, OR=1.90, 95% CI=1.60-2.25, P=2.03×10-13; LASSO, OR=1.91, 95% CI=1.65-2.21, P=3.80×10-18; adjusted for adult WHR: IVW, OR=1.80, 95% CI=1.40-2.31, P=4.20×10-6; LASSO, OR=1.90, 95% CI=1.56-2.32, P=2.76×10-10).InterpretationOur comprehensive analysis illustrated the hazard effect of obesity-related exposures for DN. In addition, we showed that childhood obesity plays a separate function in influencing the risk of DN and that the adverse effects of adult obesity (adult BMI and adult WHR) can be substantially attributed to it. Thus, several obesity-related traits deserve more attention and may become a new target for the prevention and treatment of DN and warrant further clinical investigation, especially in childhood obesity.</p

Mean cross-sectional area of soleus muscle fibers in the experimental groups.

<p>Data are expressed as the mean ± SD, scan bars: 50 µm. **p<0.01 versus Control; ^#p<0.05 versus LPD+KA. NPD, normal protein diet; LPD, low-protein diet; LPD+KA, low-protein diet supplemented with ketoacids.</p

Urinary protein and biochemical parameters in the experimental groups.

<p>Urinary protein (A), blood glucose (B), BUN(C), Scr (D) and serum albumin levels (E) in Wistar and GK rats fed with NPD, LPD and LPD+KA. Data are expressed as the mean ± SD, ^**p<0.01 versus NPD, LPD and LPD+ KA; ^#p<0.05 versus LPD+ KA; ^&&p<0.01 versus LPD and LPD+ KA. BUN, blood urea nitrogen; Scr, serum creatinine; NPD, normal protein diet; LPD, low-protein diet; LPD+KA, low-protein diet supplemented with ketoacids.</p

HE staining of the soleus muscle in the experimental groups.

<p>Representative HE stain images the control group (A), NPD group (B), LPD group (C) and LPD+KA group (D). NPD, normal protein diet; LPD, low-protein diet; LPD+KA, low-protein diet supplemented with ketoacids.</p

Protein expressions of the autophagy markers in the experimental groups.

<p>Representative western blotting analyses and group data of Beclin-1 (A), Bnip3 (B), p62 (C), and Cathepsin L (D) abundance in the soleus muscle of the experimental groups. Data are expressed as the mean ± SD, *p<0.05 versus Control; ^**p<0.01 versus Control; ^#p<0.05 versus LPD+KA; ^##p<0.01 versus LPD+KA. LPD, NPD, normal protein diet; low-protein diet; LPD+KA, low-protein diet supplemented with ketoacids.</p

Body weight loss and soleus muscle mass loss in the experimental groups.

<p>Means ± SEM of Body weight (A) and soleus muscle mass (B) of Wistar rats and GK rats fed with NPD, LPD and LPD+KA. Data are expressed as the mean ± SD, ^**p<0.01 versus Control group; ^#p<0.05 versus LPD+KA; ^##p<0.01 versus LPD+KA. NPD, normal protein diet; LPD, low-protein diet; LPD+KA, low-protein diet supplemented with ketoacids; NPD, normal protein diet.</p