Sponge-Like Porous-Conductive Polymer Coating for Ultrastable Silicon Anodes in Lithium-Ion Batteries.

Urgent calls for reversible cycling performance of silicon (Si) requires an efficient solution to maintain the silicon-electrolyte interface stable. Herein, a conductive biphenyl-polyoxadiazole (bPOD) layer is coated on Si particles to enhance the electrochemical process and prolong the cells lifespan. The conformal bPOD coatings are mixed ionicelectronic conductors, which not only inhibit the infinite growth of solid electrolyte interphase (SEI) but also endow electrodes with outstanding ion/electrons transport capacity. The superior 3D porous structure in the continuous phase allows the bPOD layers to act like a sponge to buffer volume variation, resulting in high structural stability. The in situ polymerized bPOD coating and it-driven thin LiF-rich SEI layer remarkably improve the lithium storage performance of Si anodes, showing a high reversible specific capacity of 1600 mAh g-1 even after 500 cycles at 1 A g-1 along with excellent rate capacity of over 1500 mAh g-1 at 3 A g-1 . It should be noticed that a long cycle life of 800 cycles with 1065 mAh g-1 at 3 A g-1 can also be achieved with a capacity retention of more than 80%. Therefore,  we  believe this unique polymer coating design paves the way for the widespread adoption of next-generation lithium-ion batteries.

Mannose phosphate isomerase gene mutation leads to a congenital disorder of glycosylation: A rare case report and literature review.

We report the case of a 2-year-old girl who was diagnosed with Mannose-6-phosphate isomerase-congenital disorder of glycosylation (MPI-CDG) and provide a review of the relevant literature. The young girl presented with recurrent unexplained diarrhea, vomiting, hypoproteinemia, and elevated liver transaminases. Whole-exome sequencing revealed that the patient had compound heterozygous mutations in the MPI gene (NM_0024). An exon 4 (c.455G > T, p.R152l) mutation was inherited from the mother and an exon 7 (c.884G > A, p.R295H) mutation from the father. One week after the start of mannose treatment, the vomiting and diarrhea symptoms disappeared completely and did not show any side effects. We also provide a brief review of the relevant literature. Including the present case, a total of 52 patients from hospitals across 17 countries were diagnosed with MPI-CDG. Age at disease onset ranged from birth to 15 years, with an onset under 2 years in most patients (43/50). Overall, patients presented with at least one or more of the following symptoms: chronic diarrhea (41/46), vomiting (23/27), hepatomegaly (39/44), hepatic fibrosis (20/37), protein-losing enteropathy (30/36), elevated serum transaminases (24/34), hyperinsulinemic-hypoglycemia (24/34), hypoalbuminemia (33/38), prolonged coagulation (26/30), splenomegaly (13/21), non-pitting edema (14/20), failure to thrive (13/36), portal hypertension (4/9), epilepsy (2/17), thrombosis (12/14), and abnormally elevated leukocytes (5). None of the patients was reported to have an intellectual disability (0/28). The majority of patients (26/30) showed clinical symptoms, and laboratory results improved after oral mannose administration. Our findings suggest that MPI-CDG should be considered in children with unexplained recurrent digestive and endocrine systems involvement, and gene examination should be performed immediately to obtain a definite diagnosis in order to begin treatment in a timely manner.

Study on the activity of recombinant mutant tissue-type plasminogen activator fused with the C-terminal fragment of hirudin.

In the present study, bifunctional fusion proteins were designed by fusing the kringle 2 and protease domains of tissue-type plasminogen activator (tPA) to the C-terminal fragment of hirudin. The thrombolytic and anticoagulant activities of these recombinant proteins from mammalian cells were investigated using in vitro coagulation models and chromogenic assays. The results showed that all assayed tPA mutants retained catalytic activity. The C-terminal fragment of hirudin may have weak affinity to thrombin and thus was insufficient to suppress thrombin-mediated fibrin agglutination. The strength of the thrombolytic activity only relied on the selected tPA sequences, and the fibrinolytic efficiency of single-chain protein significantly decreased. Our data indicate that truncated tPA combined with a hirudin peptide may provide a framework for the further development of a new antithrombotic agent.

Meta-Analysis of Adiponectin as a Biomarker for the Detection of Metabolic Syndrome.

Previous studies revealed the potential significance of circulating adiponectin levels with respect to the diagnosis and prediction of metabolic syndrome, but uncertainty has been noted across different cohorts. Systematic evaluation was performed for diagnostic accuracy and predictivity of adiponectin variation for metabolic syndrome in enrolled studies including 1,248 and 6,020 subjects, respectively. Adiponectin can identify metabolic syndrome with moderate accuracy (area under the curve = 0.81, 95% CI: 0.77-0.84). Heterogeneity analysis revealed that an increasing index of insulin resistance was independently associated with improving the performance of adiponectin upon metabolic syndrome diagnosis (ratio of diagnostic odds ratio = 3.89, 95% CI: 1.13-13.9). In addition, reductions in adiponectin were associated with increasing metabolic syndrome incidence in a linear dose-response manner. The risk of hypoadiponectinemia with metabolic syndrome was especially increased in men (P < 0.05). Further Mendelian randomization analysis identified that the amplified risk could be attributed to increased susceptibility (up to 7%) to insulin resistance compared with women. In conclusion, adiponectin measurement might have potential benefits in the detection of metabolic syndrome. Factors that affect insulin resistance should be considered for adjustment in future assessments.

The TORC1-Sch9-Rim15 signaling pathway represses yeast-to-hypha transition in response to glycerol availability in the oleaginous yeast Yarrowia lipolytica.

The yeast-to-hypha dimorphic transition is important for survival under nutrient starvation in fungi. The oleaginous yeast Yarrowia lipolytica grows in the oval-shaped yeast form in glycerol media whereas it adopts a filamentous form in glucose media. It is not clear why this yeast responds differently to glycerol and glucose. Here, we show that glycerol blocks dimorphic transition even in the presence of glucose whereas glycerol depletion induces filamentous growth, suggesting that dimorphic transition is repressed in response to glycerol availability. We show that the repression of dimorphic transition in glycerol media is mediated by the TORC1-Sch9 signaling pathway as both TORC1 inhibition and the loss of YlSch9 cause hyperfilamentation. TORC1-Sch9 signaling inhibits the nuclear translocation of YlRim15, a protein kinase that positively regulates filamentous growth, preventing it from entering the nucleus to activate the transcription of genes implicated in filamentous growth. Interestingly, TORC1-Sch9 signaling appears not to inhibit YlRim15 in glucose media, which could explain why Y. lipolytica responds differently to glycerol and glucose. We identified MHY1, a transcription factor-encoding gene known to be critical for filamentous growth, as one target regulated by the TORC1-Sch9-Rim15 signaling pathway. Our results provide new insights in the regulation of dimorphic transition in yeast.