Amelioration of obesity and inflammation by polysaccharide from unripe fruits of raspberry via gut microbiota regulation.

Raspberry, a traditional medicine food homology species, has important benefits in patients with metabolic syndrome. However, the mechanism of raspberry polysaccharides (RP) on obesity remains unclear. In our study, we showed that RP intervention is negatively associated with body weight gain, hyperlipidemia, inflammation, and fat accumulation in obese mice. RP ameliorated HFD-induced gut microbiota dysbiosis, produced short-chain fatty acids, maintained intestinal barrier integrity, and prevented metabolic endotoxemia, manifested by decreased host lipopolysaccharide level, and increased colon expression of tight junction proteins. These effects might be related with driven by a SCFAs-producing bacterium and downregulation of TLR4/NF-κB signaling transduction. Notably, the abundance of Ruminococcaceae_UCG - 014, Lactobacillus taiwanensis, Bifidobacterium pseudolongum, and Turicibacter are markedly correlated with enhanced intestinal barrier function induced by RP treatment. Thus, we believe that RP could be as a potential health supplement or prebiotic for obesity therapy.

Corrosion Resistance of Amorphous-Nanocrystalline Composite Structure Materials.

The purpose of this paper is to investigate the corrosion resistance of different nanoscale microstructures in the same material system and propose a novel method to obtain high-performance materials. During the last 2 decades, microstructure refinement and microalloying have become the main methods to prepare high-performance materials. The tensile strength of nanocrystalline solid solutions can reach 2.3 gigapascal, which is more than 1 fold the strength of traditional steel. However, there are few studies about the corrosion resistance of different nanoscale microstructures. In this paper, coatings with different microstructures (nanocrystalline, amorphous, and amorphous-nanocrystalline composite) have been successfully prepared by electrodeposition in the same material system (nickel-phosphorus alloy). Electrochemical test and high-pressure corrosion immersion test were carried out. The results show that the material loss of amorphous-nanocrystalline coating (P = 9.2 wt %) is about 1/4 that of crystalline coating at 8 MPa. In the range of 0.1 and 8 MPa, the average acceleration effect of hydrostatic pressure on the corrosion rate was calculated to be 1.611 × 10-6 g·cm-2·d-1·MPa-1.

Long non-coding RNA PTENP1 inhibits proliferation and migration of breast cancer cells via AKT and MAPK signaling pathways.

We aimed to investigate the influence of long non-coding RNA (lncRNA) PTEN pseudogene-1 (PTENP1) on the proliferation, migration and cycle of breast cancer cells and its mechanism. Lentiviral vectors expressing PTENP1 were synthesized and breast cancer cells MCF7 were transfected with LV003-GFP-PTENP1 and LV003-GFP, respectively. The proliferation capacities of breast cancer cells were detected using CCK-8 assay, and the migration capacities of breast cancer cells were detected using scratch assay; flow cytometry was used to detect the cell cycles and Western blot was used to detect the expression levels of cyclin A2, CDK2, p-p44/42 MAPK, t-p44/42 MAPK, p-p38 MAPK, t-p38 MAPK, p-AKT, t-AKT in AKT and MAPK pathways. The absorbance values (A450) of cells in experimental group at 48 and 72 h were 1.4±0.3 and 2.3±0.47, respectively, which were significantly lower than those in control group (3.2±0.39, 3.4±0.58) (P<0.05). The number of cell colonies in experimental group was (48±13), which was significantly lower than that in control group (159±16) (P<0.01). The cell migration rate in experimental group was 22.8±3.3%, which was significantly lower than that in control group 61.8±5.2% (P<0.01). Western blot detection showed that the expression levels of cyclin A2, CDK2, p-AKT, p-p44/42 MAPK and p-p38 MAPK in experimental group were significantly decreased compared with those in control group. LncRNA PTENP1 can inhibit the proliferation and migration of breast cancer cells via the AKT and MAPK signaling pathways.

Aesthetic principles access thyroidectomy produces the best cosmetic outcomes as assessed using the patient and observer scar assessment scale.

BACKGROUND: Thyroid carcinoma (TC) is more likely to occur in young women. The aim of this study was to compare the aesthetic effect of different thyroidectomies. METHODS: One hundred twenty female patients who underwent thyroidectomy were evenly distributed into three groups: conventional access (CA), aesthetic principles access (APA) and minimally invasive access (MIA). The Patient and Observer Scar Assessment Scale (POSAS) was used as the assessment tool for the linear scar. RESULTS: The patients in the MIA group showed significantly less intraoperative blood loss, less drainage, a shorter scar length and a shorter duration of drainage than those in the CA group and the APA group. However, the operation time of 129.0 min in the MIA group was significantly longer than the 79.6 min in the CA group and the 77.0 min in the APA group. The best aesthetic score, as assessed by the Observer Scar Assessment Scale (OSAS), was obtained in the APA group. The Patient Scar Assessment Scale (PSAS) scores were significantly lower in the APA group and CA group than in the MIA group. Significantly lower objective scar ratings were found in the APA group than in the other two groups. CONCLUSION: These results show that APA produced the best surgical outcomes in TC patients, indicating that conventional thyroidectomy can produce an ideal aesthetic result using the principles of aesthetic surgery. Thyroid surgery need not be performed through excessively short incisions for the sake of patient satisfaction with the scar's appearance. TRIAL REGISTRATION: This clinical trial was retrospectively registered on ClinicalTrials.gov PRS on August 1st,2017 ( NCT03239769 ).

Persistent Expression of VCAM1 in Radial Glial Cells Is Required for the Embryonic Origin of Postnatal Neural Stem Cells.

During development, neural stem cells (NSCs) undergo transitions from neuroepithelial cells to radial glial cells (RGCs), and later, a subpopulation of slowly dividing RGCs gives rise to the quiescent adult NSCs that populate the ventricular-subventricular zone (V-SVZ). Here we show that VCAM1, a transmembrane protein previously found in quiescent adult NSCs, is expressed by a subpopulation of embryonic RGCs, in a temporal and region-specific manner. Loss of VCAM1 reduced the number of active embryonic RGCs by stimulating their premature neuronal differentiation while preventing quiescence in the slowly dividing RGCs. This in turn diminished the embryonic origin of postnatal NSCs, resulting in loss of adult NSCs and defective V-SVZ regeneration. VCAM1 affects the NSC fate by signaling through its intracellular domain to regulate ß-catenin signaling in a context-dependent manner. Our findings provide new insight on how stem cells in the embryo are preserved to meet the need for growth and regeneration.

Interaction Between Gastric Carcinoma Cells and Neural Cells Promotes Perineural Invasion by a Pathway Involving VCAM1.

BACKGROUND: Perineural invasion (PNI) is one of the important routes for local spread of gastric carcinoma associated with poor prognosis. However, the exact cellular characteristics and molecular mechanisms of PNI are still unclear. AIM: To identify the interaction between gastric carcinoma cells and neural cells, and whether vascular cell adhesion molecule-1 (VCAM1) is involved in this process. METHODS: We adopted in vitro cell coculture assays to investigate the cellular and molecular interaction between gastric cancer cells and neural cells. RESULTS: We find upregulation of VCAM1 in clinical gastric cancer tissue samples. In in vitro tumor-neural cell coculture system, gastric cancer cells with high level of VCAM1 promote proliferation of neural progenitor cells and induce the process outgrowth and branching of neural cells. Reciprocally, neural cells enhance neurotropic migration and mobility of tumor cells. Repressing VCAM1 function through VCAM1 blocking antibody can attenuate these effects. CONCLUSIONS: Our study indicates that VCAM1 is significantly involved in tumor invasion via mediating nerve-tumor interaction, which is a mutually beneficial process. It is possible that interaction between neural cells and tumor cells might contribute to PNI of gastric carcinoma. Inhibiting the activity of VCAM1 could be a potential strategy targeting PNI in gastric carcinoma therapy.

[Cellular and molecular mechanisms of perineural Invasion in gastric cancer].

Perineural invasion(PNI) is one of the important routes for metastasis of gastric carcinoma and results in local recurrence and cancer pain after radical gastrectomy. The dismal prognosis of gastric cancer has been intimately associated with lymph node metastasis, hematogenous metastasis that partly caused by PNI. Nerve, vascular and lymphatic constitutes the tumor microenvironment which plays a decisive role in the development of cancer. Molecular interaction and morphological change contribute to reciprocal signaling interactions between tumor cell and nerve. However, the underlying mechanism of PNI in gastric cancer is still unclear and needs further study. Here, we present a brief review of literatures on the topic of PNI in gastric cancer.

Not all side population cells contain cancer stem-like cells in human gastric cancer cell lines.

INTRODUCTION: Side population (SP) cells may play a crucial role in tumorigenesis and the recurrence of cancer. Many kinds of cell lines and tissue have demonstrated presence of SP cells including different gastric cancer cell lines. However, is that true all SP cells contain cancer stem-like cells in gastric cancer cell lines? MATERIALS AND METHODS: MKN-45 and BGC-823 cells labeled with Hoechst 33342 were chosen to obtain SP cells, then characterized the cancer stem-like properties of SP cells both in vitro and in vivo. Five stemness-related genes expression profiles, including OCT-4, SOX-2, NANOG, CD44 and ATP-binding cassette transporters gene ABCG-2, were tested in SP and MP cells using quantitative real-time RT-PCR. Western blot was chosen to show the difference of protein expression between SP and MP cells. When inoculated into non-obese diabetic/severe combined immunodeficiency (NOD/SCID) mice, SP cells from MKN-45 showed higher tumorigenesis tendency than MP cells, but SP cells from BGC-823 showed same tumorgenesis tendency as MP cells. CONCLUSION: SP cells from MKN-45 possess cancer stem cell properties and proved that they were gastric cancer stem-like cells. SP cells from BGC-823 didn't possess cancer stem cell properties and proved that not all SP cells contain cancer stem-like cells in gastric cancer cell lines.