A Novel Approach of Sea Urchin-like Fe-Doped Co3O4 Microspheres for Li-S Battery Enables High Energy Density and Long-Lasting.

The poor cycle stability caused by the shuttle effect of polysulfides which have been key scientific issue in the development of high-efficiency lithium-sulfur (Li-S) batteries. In this work, the authors report a Fe-doped Co3O4 (named FCO) that was used as a sulfur-loaded host material for Li-S batteries. We demonstrate the important roles of well-designed Co3O4 particles and Fe atoms in regulating polysulfide conversion due to the strong adsorption of polysulfides by polar Co3O4, whereas Fe atoms and Co3O4 catalyze polysulfide conversion. Therefore, the LiS batteries with FCO-180 (When the hydrothermal temperature is 180 °C) sea urchinlike composites exhibited a high superior energy density (992.7 mAh g-1 at 0.2 C, after 100 cycles) and long-term cyclability (649.4 mAh g-1 at 1 C, 300 cycles) with high sulfur loading (75 wt%). This work confirms that the FCO-180 sea urchinlike increases not only the capacity of high-rate but also a generic and feasible strategy to construct practical Li-S batteries for emerging energy-storage applications.

[Genetic variant analysis of a pedigree affected with lymphedema-distichiasis syndrome].

OBJECTIVE: To analyze FOXC2 gene variant in a family affected with lymphodema-distichiasis syndrome (LDS). METHODS: Peripheral blood samples were collected for the extraction of DNA and protein. Whole-exome sequencing was carried out to detect variants in the proband. Suspected variant was validated by Sanger sequencing. Western blotting was used to detect changes in protein expression. RESULTS: The proband and his mother were both found to carry a heterozygous nonsense variant c.177C>G (p.Tyr59X) of the FOXC2 gene, which was previously unreported. Down-regulated expression of FOXC2 was detected by Western blotting. Prenatal ultrasonography of the fetus indicated increased nuchal thickness. Amniocentesis was performed at 21+1 weeks of pregnancy, genetic testing suggested that the fetus also carried the c.177C>G variant. CONCLUSION: The patients' condition may be attributed to the heterozygous nonsense variant c.177C>G of the FOXC2 gene, which resulted in a significant decrease in FOXC2 expression. Increased nuchal thickness may also be related with decreased FOXC2 expression. Above finding has expanded the variant spectrum of the FOXC2 gene.

[Identification of a Tp63 gene variant in an abortus with Ectrodactyly, Ectodermal dysplasia, Cleft lip/palate syndrome by whole-exome sequencing].

OBJECTIVE: To detect potential variant in a male fetus suspected for Ectrodactyly, Ectodermal dysplasia, Cleft lip/palate (EEC) syndrome. METHODS: Peripheral blood samples of the fetus and his parents were collected for the extraction of DNA. Whole-exome sequencing was carried out to detect potential variants. Suspected variants were verified by Sanger sequencing. RESULTS: The fetus was found to carry a heterozygous c.673C>T missense variant of the Tp63 gene, which was known to underlie split-hand/split-foot malformation. The same variant was not found in either parents. CONCLUSION: The heterozygous c.673C>T missense variant of the Tp63 gene probably underlies the EEC syndrome in the fetus. Above finding also expanded the phenotypic spectrum for this variant.

Human umbilical cord-derived mesenchymal stem cells ameliorate the enteropathy of food allergies in mice.

Food allergy prevalence has steadily increased worldwide over the past decades and immunotherapeutic treatment strategies are gaining attention. Human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) exhibit similar immune regulatory properties to bone marrow-derived MSCs. hUC-MCSs can be prepared with fewer ethical constraints and are potential candidates for allergic disorder therapies. The current study aimed to investigate potential antiallergic properties of hUC-MSCs in mice with ovalbumin (OVA)-induced food allergy. Administration of hUC-MSCs cells intraperitoneally combined with oral gavage of the culture medium significantly alleviated OVA-induced diarrhea symptoms. Additionally, this treatment significantly decreased IgE levels and the percentage of T helper 2 cells in the blood, which were increased in mice with OVA-induced food allergy. The mRNA levels of the inflammatory cytokines interleukin-4 and tumor necrosis factor-α, and inflammatory cell infiltration in mouse colons were significantly decreased in hUC-MSCs-treated animals compared with mice with OVA-induced food allergy. Goblet cells were detected in colons of allergy-induced mice and their numbers were reduced following treatment with hUC-MSCs. In addition, treatment with hUC-MSCs reestablished the gut flora. The results revealed that hUC-MSCs may have a potential application in food allergy therapy.

Butyrate upregulates the TLR4 expression and the phosphorylation of MAPKs and NK-κB in colon cancer cell in vitro.

Microbiota and its induced inflammation in colorectal mucosa have been considered risk factors for the development of colorectal carcinogenesis. Previous studies demonstrated that the coexisting elements of microbiota in the gut, such as short chain fatty acids (SCFAs) and lipopolysaccharides (LPS), which exhibited regulatory effects on the intestinal epithelial cells individually. Unfortunately, the association between butyrate and the toll-like receptor (TLR) signaling pathway in the development of colon cancer is not fully elucidated. In the present study, by culturing human colon cancer SW480 cells or mouse colon cancer CT26 cells with butyrate and/or TLR4 ligand LPS in vitro, it was identified that butyrate suppressed the growth and promoted apoptosis of these cancer cells. Notably, the expression levels of TLR4 and CD14 were markedly increased on these butyrate-treated cells, but not on LPS-alone treated cells. Additionally, butyrate treatment induced the phosphorylation of extracellular signal-regulated kinase, tumor protein 38, c-Jun NH2-terminal kinase and nuclear factor-κB (NF-κB) p65, and then promoted the pro-inflammatory cytokine tumor necrosis factor-α, but not interleukin 6 secretion in SW480 and CT26 cells. Therefore, butyrate treatment regulates the expression of TLR4, mitogen-activated protein kinase and NF-κB signal pathway activation and pro-inflammatory response in vitro. Although the exact mechanisms have not been fully explored, these results suggested that butyrate and LPS-TLR4 signaling mediated innate immunity in colon cancer cells through two distinct but inter-regulated pathways. Thus, butyrate can further initiate innate immunity against tumor cells by upregulating the TLR4 expression and activation to preserve intestinal homeostasis.

High fish oil diet promotes liver inflammation and activates the complement system.

Diets rich in n-3 polyunsaturated fatty acid (n-3 PUFA) fish oil (FO) have beneficial effects in obesity­associated metabolic disease. However, contradictory roles in inflammatory disease intervention have been reported. Our previous work revealed that a high­FO diet promoted myeloid cell differentiation by modifying the bone marrow microenvironment; however, its effects on liver inflammation and complement system activation remain unknown. By performing ELISA, reverse transcription­quantitative polymerase chain reaction, flow cytometry and histology on mice fed with high­FO and low­fat diets, the present study demonstrated that a 4­week high­FO diet promoted liver inflammation in mice without affecting body or liver weight. The livers of high­FO diet mice exhibited increased infiltration of T cells and CD11b+ Gr­1+ myeloid cells. Additionally, a higher level of IL­1ß and MCP­1 mRNA expression was detected, suggesting that the high­FO diet promoted liver inflammation. Further experiments indicated that the high­FO diet increased the total hemolytic complement activity (CH50), promoted the production of the membrane attack complex and increased the levels of various complement proteins in vivo, including complement components C3, C4b, C1qb and factor B. Furthermore, higher concentrations of triglyceride were detected in the peripheral blood of high­FO diet mice, indicating the potential protective roles of n­3 PUFAs in FO against lipotoxicity in hyperlipidemia. Collectively, the present study demonstrated that high FO intake induced inflammation and activated the complement system in the liver. However, further study is required to determine the exact mechanisms.

High fat diet exacerbates dextran sulfate sodium induced colitis through disturbing mucosal dendritic cell homeostasis.

Epidemiological studies have shown that fat rich western diet contributes to the high incidence of inflammatory bowel disease (IBD). Moreover, accumulated data indicated that fat dietary factor might promote the change of the composition and metabolism in commensal flora. But, the exact mechanisms for fatty diet in gut inflammation are not well demonstrated. In this study, we found that high fat diet (HFD) promoted inflammation and exacerbated the disease severity of dextran sulfate sodium (DSS) induced colitis in mice. Compared with low fat diet (LFD)/DSS mice, shorter colon length, more epithelial loss and crypt destruction and more Gr-1+ myeloid inflammatory cells infiltration in colons were observed in HFD/DSS cohorts. Interestingly, such HFD mediated inflammation accompanied with the dys-regulation of hematopoiesis, and more hematopoiesis stem and progenitor cells were detected in colon and spleen. We further analyzed the effects of HFD and DSS treatment on mucosal DC subsets, and found that DSS treatment in LFD mice mainly dramatically increased the percentage of CD11c+CD103-CD11b+ DCs in lamina propria (LP). While, in HFD/DSS mice, HFD pre-treatment not only increased the percentage of CD11c+CD103-CD11b+ DCs, but also decreased CD11c+CD103+CD11b+ in both LP and mesenteric lymph nodes (MLN) in mice with colitis. This disequilibrium of mucosal dendritic cells in HFD/DSS mice may depend on the reduced levels of buytrate and retinoic acid. Thus, this study declared the effects of HFD on gut microenviroment, and further indicated its potential role in the development of DSS induced colitis.

Purification of hen egg white ovomacroglobulin using one-step chromatography.

Hen egg white (EW) are one of the most ideal sources of active proteins, and ovomacroglobulin, as a protease inhibitor, has been demonstrated to possess numerous biological properties including antibacterial and anti-inflammatory properties as well as activity for the treatment of keratitis. The objective of this study was to develop a simple and rapid method for the purification of ovomacroglobulin from hen EW on a laboratory scale. Hen EW was diluted with an equal volume of distilled water followed by a two-step PEG precipitation to remove ovomucin and to obtain ovomacroglobulin-rich precipitate. The precipitate was dissolved and further purified by gel filtration chromatography. Ovomacroglobulin was collected with a purity of 97.0 ± 0.3% by HPLC and a yield of 62.5%. The atomic force microscopy images showed that ovomacroglobulin molecules on a mica surface emerged as an "oval-shaped plate" with a molecular volume of 1536.9 ± 330.0 nm(3) , indicating that purified ovomacroglobulin has an integrated molecular structure. With the improvement of PEG precipitation and the simplification of the chromatography, the whole purification process could be finished well within one working day. This protocol has an advantage of rapidity, and would facilitate studies of ovomacroglobulin.