Adsorption characteristics of S-Metolachlor onto the sawdust biochar derived from Acacia auriculiformis.

The adsorption mechanism of S-Metolachlor in an aqueous solution by sawdust biochar derived from Acacia auriculiformis (SAB) was studied. SAB was manufactured at 500 °C for 4 h under oxygen-limited conditions and characterized for SEM, EDS, pHpzc, BET, and FTIR. The adsorption kinetics, isotherm, and diffusion studies of S-Metolachlor and SAB were further explored. Moreover, the effects of the solution pH were examined on the adsorption of S-Metolachlor by SAB. The BET analysis of SAB was achieved at 106.74 m2.g-1 and the solution pH did not significantly influence the S-Metolachlor adsorption. The adsorption data were fitted into a Langmuir isotherm and the PSO model. The film diffusion coefficient Df (4.93 × 10-11 to 8.17 × 10-11 m2.s-1) and the particle diffusion coefficient Dp (1.68 × 10-11 to 2.65 × 10-11 m2.s-1) were determined and the rate-limiting step of S-Metolachlor adsorption and SAB was governed by liquid film diffusion. The S-Metolachlor adsorption process onto SAB was controlled by multiple mechanisms, including pore filling, H-bonding, hydrophobic interaction, and π-π EDA interactions. H-bonding is the main interaction for the adsorption of S-Metolachlor and SAB. Conclusively, the study illustrates that biochar produced from Acacia auriculiformis sawdust possessed effective adsorption properties for S-Metolachlor herbicide.

Stunting and Overweight among 12-24-Month-Old Children Receiving Vaccination in Ho Chi Minh City, Vietnam.

INTRODUCTION: Malnutrition and obesity are a double burden on children in developing countries and could induce higher risks of noncommunicable diseases in the long term. In the big cities of Vietnam, both issues are present and share the issue of nutrition problems; the prevalence of malnutrition in children is gradually decreasing while the prevalence of obesity is increasing rapidly. The paper aims to identify the prevalence of stunting and overweight/obesity in apparently healthy young children in Ho Chi Minh City (HCMC). METHODS: A prospective cross-sectional study recruited 12-24-month-old children receiving national vaccination in community health centers in HCMC from February 2016 to July 2017. Sixteen healthcare centers were randomly selected among 8 districts of HCMC. Stunting and overweight were defined by height-for-age z-score <-2 SD and BMI z-score ≥+2 SD. RESULTS: A total of 768 children had mean age of 16.8±4.2 months old, 51.7% boys. The prevalence of stunting and overweight/obesity was 8.2% and 10.7%, respectively. Stunting was associated with older age, boys, and low birth weight of children and occupation of mothers (P <0.05). No associated risk factor was observed for overweight/ obesity status. CONCLUSION: The prevalence of overweight/obesity was higher than the prevalence of stunting in 12-24-month-old children in HCMC. Overweight/obesity would be a public health problem for children in big cities.

Three novel mutations in the ATP7B gene of unrelated Vietnamese patients with Wilson disease.

BACKGROUND: Wilson disease (OMIM # 277900) is a autosomal recessive disorder characterized by accumulation of copper in liver and brain. The accumulation of copper resulting in oxidative stress and eventually cell death. The disease has an onset in a childhood and result in a significant neurological impairment or require lifelong treatment. Another serious consequence of the disease is the development of liver damage and acute liver failure leading to liver transplant. The disorder is caused by mutations in the ATP7B gene, encoding a P-type copper transporting ATPase. CASE PRESENTATION: We performed genetic analysis of three unrelated patients from three different Vietnamese families. These patients had clinical features such as numbness of hands and feet, vomiting, insomnia, palsy, liver failure and Kayser-Fleischer (K-F) rings and were diagnosed with Wilson disease in the Human Genetics Department, Vietnam National Children's Hospital. The entire coding region and adjacent splice sites of ATP7B gene were amplified and sequenced by Sanger method. Sequencing data were analyzed and compared with the ATP7B gene sequence published in Ensembl (ENSG00000123191) by using BioEdit software to detect mutations. CONCLUSIONS: In this study, five mutations in the ATP7B gene were found. Among of these, three mutations were novel: c.750_751insG (p.His251Alafs*19) in exon 2, c.2604delC (p.Pro868Profs*5) in exon 11, and c.3077 T > A (p.Phe1026Tyr) in exon 14. Our results of the mutations associated with Wilson disease might facilitate the development of effective treatment plans.

Chimeric RNA/ethylene-bridged nucleic acids promote dystrophin expression in myocytes of duchenne muscular dystrophy by inducing skipping of the nonsense mutation-encoding exon.

Editing of dystrophin mRNA by induction of exon skipping, using antisense oligonucleotides, has been proposed as one way to generate dystrophin expression in Duchenne muscular dystrophy (DMD) patients. Here, antisense chimeric oligonucleotides consisting of RNA and a new modified nucleic acid are tested for activity to induce skipping of an exon containing a nonsense mutation. In a Japanese DMD case, a nonsense mutation (R1967X) due to a single nucleotide change in exon 41 of the dystrophin gene (C5899T) was identified. Oligonucleotides consisting of 2'-O-methyl RNA and a new 2'-O,4'-C-ethylene-bridged nucleic acid (ENA) were designed to bind the mutation site of exon 41, and their ability to induce exon 41 skipping in dystrophin mRNA was evaluated. Finally, among the specific oligonucleotides tested, an 18-mer RNA/ENA chimera was found to have the strongest activity, inducing exon 41 skipping in nearly 90% of dystrophin mRNA. Accordingly, nearly 90% of cultured myocytes were shown to be dystrophin positive by immunohistochemical analysis. Western blot analysis disclosed the presence of nearly normal-sized dystrophin up to 1 week after the transfection. Our results suggest that an RNA/ENA chimera can be used to express dystrophin in DMD.