Cut-off voltage influencing the voltage decay of single crystal lithium-rich manganese-based cathode materials in lithium-ion batteries.

The voltage decay of Li-rich layered oxide cathode materials results in the deterioration of cycling performance and continuous energy loss, which seriously hinders their application in the high-energy-density lithium-ion battery (LIB) market. However, the origin of the voltage decay mechanism remains controversial due to the complex influences of transition metal (TM) migration, oxygen release, indistinguishable surface/bulk reactions and the easy intra/inter-crystalline cracking during cycling. We investigated the direct cause of voltage decay in micrometer-scale single-crystal Li1.2Mn0.54Ni0.13Co0.13O2 (SC-LNCM) cathode materials by regulating the cut-off voltage. The redox of TM and O2- ions can be precisely controlled by setting different voltage windows, while the cracking can be restrained, and surface/bulk structural evaluation can be monitored because of the large single crystal size. The results show that the voltage decay of SC-LNCM is related to the combined effect of cation rearrangement and oxygen release. Maintaining the discharge cutoff voltage at 3 V or the charging cutoff voltage at 4.5 V effectively mitigates the voltage decay, which provides a solution for suppressing the voltage decay of Li-rich and Mn-based layered oxide cathode materials. Our work provides significant insights into the origin of the voltage decay mechanism and an easily achievable strategy to restrain the voltage decay for Li-rich and Mn-based cathode materials.

Chronic folate deficiency induces glucose and lipid metabolism disorders and subsequent cognitive dysfunction in mice.

Previous studies have shown that folate levels were decreased in patients with type 2 diabetes (T2D) and further lowered in T2D patients with cognitive impairment. However, whether folate deficiency could cause T2D and subsequent cognitive dysfunction is still unknown. The present study aimed to explore the effects of chronic folate deficiency (CFD) on glucose and lipid metabolism and cognitive function in mice. Seven-week-old mice were fed with either a CFD or control diet for 25 weeks. Serum folate was significantly reduced, whereas serum total homocysteine was significantly increased in the CFD group. Moreover, CFD induced obesity after a 6-week diet treatment, glucose intolerance and insulin resistance after a 16-week-diet treatment. In addition, CFD reduced the hepatic p-Akt/Akt ratio in response to acute insulin administration. Moreover, CFD increased serum triglyceride levels, upregulated hepatic Acc1 and Fasn mRNA expression, and downregulated hepatic Cd36 and ApoB mRNA expression. After a 24-week diet treatment, CFD induced anxiety-related activities and impairment of spatial learning and memory performance. This study demonstrates that folate deficiency could induce obesity, glucose and lipid metabolism disorders and subsequent cognitive dysfunction.

[Responses of diurnal variation of flag-leaf photosynthesis and photosynthetic pigment content to elevated atmospheric CO2 concentration and temperature of Japonica rice during late growth stage: A FACE study.] / ç²³ç¨»ç”Ÿè‚²åŽæœŸå‰‘å¶å ‰åˆæ—¥å˜åŒ–å’Œå ‰åˆè‰²ç´ å¯¹å¤§æ°”CO2浓度和温度升高的响应­­FACEç ”ç©¶.

A local popular Japonica rice (Oryza sating L.) cultivar, Nanjing 9108, was tested with free air controlled enrichment (FACE) approach to study the responses of photosynthetic pigment content and diurnal variation of flag-leaf photosynthesis to elevated atmospheric CO2 concentration and temperature. Four alternative treatments were designed with two CO2 concentration levels (ambient and elevated 200 µmol·mol-1) and two air temperature regimes (ambient and elevated 1-2 ℃). Diurnal variation of flag-leaf photosynthesis was measured in the middle full stage and the late full stage, and photosynthetic pigment of the leaf was analyzed afterward. Results showed that diurnal variation of net photosynthetic rate (Pn) in each treatment followed a double-peak curve with midday depression feature during late growth stage. Compared to Pn under ambient condition, Pn under elevated CO2 concentration increased by 47.6% and 39.1% on average at middle full stage and late full stage, respectively. There was a negative correlation between temperature and Pn with no significance. Both elevated CO2 concentration and temperature had a significant negative effect on stomatal conductance (gs), decreased by 17.0% and 11.8% on average, respectively. Elevated CO2 concentration significantly reduced transpiration rate (Tr), chlorophyll a (Chl a), chlorophyll b (Chl b), carotene (Car), total chlorophyll (Chl t) and chlorophyll a/b ratio (Chl a/b) during late growth stage of rice by 5.9%, 50.4%, 21.3%, 41.4%, 39.4% and 21.4% on average, respectively, whereas water use efficiency (WUE) increased by 47.9%. However, there were opposite effects on Tr, WUE and photosynthetic pigment content under elevated temperature, with Tr increased by 10.2% and WUE decreased by 20.4%. It could be concluded that elevated CO2 concentration had a greater effect on Pn, gs and photosynthetic pigment content of rice leaf than elevated temperature did during late growth stage. Therefore, it should be paid more attention to the colligate effects of elevated CO2 concentration and high temperature on photosynthesis and photosynthetic pigment content to reduce negative effect of high air temperature.

Maternal lipopolysaccharide exposure results in glucose metabolism disorders and sex hormone imbalance in male offspring.

An adverse intrauterine environment may be an important factor contributing to the development of type 2 diabetes in later life. The present study investigated the longitudinal effects of maternal lipopolysaccharide (LPS) exposure during the third trimester on glucose metabolism and sex hormone balance in the offspring. Pregnant mice were intraperitoneally injected with LPS (50 µg/kg) daily from gestational day (GD) 15 to GD17. Glucose tolerance test (GTT) and insulin tolerance test (ITT) were assessed at postnatal day (PND) 60 and PND120. Sex hormones, their receptors, and metabolic enzymes (aromatase) were measured in male offspring at different phases of development (PND14: juvenile; PND35: adolescence; PND60: adulthood; and PND120: middle age). LPS-exposed male offspring exhibited glucose intolerance and insulin resistance by GTT and ITT at middle age, accompanied by an increase in fasting blood glucose and reductions in serum insulin levels and hepatic phosphorylated (p) -AKT/AKT ratio. However, glucose intolerance and insulin resistance were not observed in LPS-exposed female offspring. Maternal LPS exposure upregulated hepatic aromatase proteins and mRNA levels in male offspring at all time points. At adolescence, the testosterone/estradiol ratio (T/E2) was markedly reduced in LPS-exposed male offspring. Moreover, maternal LPS exposure significantly increased hepatic estrogen receptor (ER) α expressions and decreased hepatic androgen receptor (AR) expressions in male offspring. At adulthood, maternal LPS exposure increased serum estradiol levels, decreased serum testosterone levels and elevated hepatic ERß expressions in male offspring. In conclusion, maternal LPS exposure upregulated aromatase expressions, followed by a reduction in the T/E2 ratio and an alteration in sex hormone receptor activity, which might be involved in the development of glucose metabolism disorders in middle-aged male offspring. This study provides a novel clue and direction to clarify the pathogenesis of maternal infection-related diabetes in male offspring.

Folic Acid Promotes Wound Healing in Diabetic Mice by Suppression of Oxidative Stress.

The aim of this study was to investigate the effects of folic acid on impaired wound healing in diabetic mice. Male mice were divided into three groups: group 1, the non-diabetic mice (control); group 2, the streptozotocin (STZ)-induced type 1 diabetic mice; and group 3, the diabetic mice that received a daily dose of 3 mg/kg folic acid via oral gavage. Full-thickness excision wounds were created with 8-mm skin biopsy punches. Each wound closure was continuously evaluated until the wound healed up. Wound healing was delayed in diabetic mice compared with the non-diabetic mice. There were significantly reduced levels of hydroxyproline content (indicator of collagen deposition) and glutathione in diabetic wounds, whereas levels of lipid peroxidation and protein nitrotyrosination were increased. Daily supplementation with folic acid restored diabetes-induced healing delay. Histopathology showed that folic acid supplementation accelerated granulation tissue formation, proliferation of fibroblasts, and tissue regeneration in diabetic mice. Interestingly, folic acid alleviated diabetes-induced impaired collagen deposition in wounds. Moreover, folic acid significantly decreased levels of lipid peroxidation, protein nitrotyrosination and glutathione depletion in diabetic wounds. In conclusion, our results indicate that folic acid supplementation may improve impaired wound healing via suppressing oxidative stress in diabetic mice.