Water resistant, biodegradable and flexible corn starch/carboxymethyl cellulose composite film for slow-release fertilizer coating materials.

The inherent limitations of Cornstarch (CS) and Carboxymethyl Cellulose (CMC) membranes, such as brittleness, fragility, and water solubility, limit their use in controlled-release fertilizers. This study reports on the synthesis of crosslinked CMC/CS-20-E composite membranes using the casting technique, with epichlorohydrin (ECH) as the crosslinking agent in an acidic environment to crosslink CS and CMC. The synthesized composite film demonstrates remarkable water resistance, as evidenced by the insignificant alteration in its morphology and structure post 72 h of water immersion. Its flexibility is reflected in its capacity to endure knotting and bending, with an elongation at break reaching 78.1 %. Moreover, the degradation rate surpasses 90 % within a span of seven days. The CMC/CS-20-E-x-urea controlled-release fertilizer was subsequently produced using a layer-by-layer self-assembly technique, where urea particles were incorporated into the crosslinked composite solution. This CMC/CS-20-E-x-urea controlled-release fertilizer displayed superior controlled-release performance over a duration of seven days when juxtaposed with pure urea. In particular, the CMC/CS-20-E-3 %-urea controlled-release fertilizer showed a cumulative release rate of 84 % by the seventh day. The controlled-release fertilizers developed in this study offer a promising strategy for creating eco-friendly options that are crucial for fertilizing crops with short growth cycles.

miR-210 in Exosomes Derived from Macrophages under High Glucose Promotes Mouse Diabetic Obesity Pathogenesis by Suppressing NDUFA4 Expression.

OBJECTIVE: Type 2 diabetes mellitus (T2DM) is featured by insulin resistance and lipid metabolism dysregulation. A large number of miRNAs were identified in exosomes derived from adipose tissue macrophages associated with T2DM pathogenesis, but its pathogenic roles remain unknown. This study is aimed at investigating the function of miR-210 in diabetic obesity. METHODS: Exosomes from mouse macrophage RAW264.7 cells were characterized by electron microscopy, combined with biomarker expression by western blot. Expression of miR-210 was determined by quantitative RT-PCR. Glucose uptake was measured by a fluorometric method, and the mitochondrial respiratory chain activity was evaluated by ELISA. The target gene of miR-210 was validated by dual-luciferase reporter and pull-down assays. A mouse obese diabetic model was established by a high-fat diet and streptozocin treatment. RESULTS: miR-210 was highly expressed in exosomes derived from high glucose-induced macrophage RAW264.7 cells. Macrophage-derived exosomes impaired glucose uptake and mitochondrial CIV complex activity and suppressed NADH dehydrogenase ubiquinone 1 alpha subcomplex 4 (NDUFA4) expression in 3T3-L1 adipocytes. miR-210 directly bind with mRNA sequences of NDUFA4 gene. Inhibition of miR-210 mitigated the effects of macrophage-derived exosomes on the glucose uptake and complex IV (CIV) activity in 3T3-L1 adipocytes, and NDUFA4 overexpression offset the inhibition of glucose uptake and CIV activity by macrophage-derived exosomes. Furthermore, mice with miR-210 knockout showed greatly repressed diabetic obesity development. CONCLUSION: miR-210 derived from adipose tissue macrophages promotes mouse obese diabetes pathogenesis by regulating glucose uptake and mitochondrial CIV activity through targeting NDUFA4 gene expression.