Anisotropic swelling and fracture of silicon nanowires during lithiation.

We report direct observation of an unexpected anisotropic swelling of Si nanowires during lithiation against either a solid electrolyte with a lithium counter-electrode or a liquid electrolyte with a LiCoO(2) counter-electrode. Such anisotropic expansion is attributed to the interfacial processes of accommodating large volumetric strains at the lithiation reaction front that depend sensitively on the crystallographic orientation. This anisotropic swelling results in lithiated Si nanowires with a remarkable dumbbell-shaped cross section, which develops due to plastic flow and an ensuing necking instability that is induced by the tensile hoop stress buildup in the lithiated shell. The plasticity-driven morphological instabilities often lead to fracture in lithiated nanowires, now captured in video. These results provide important insight into the battery degradation mechanisms.

Raman analysis of CdSe/CdS core-shell quantum dots with different CdS shell thickness.

We report the first-order and high-order Raman scattering from core-shell CdSe/CdS nanocrystals and investigate the evolution of the longitudinal mode of CdSe (LO1) and CdS (LO2), and the surface mode of CdSe (SO1) and CdS (SO2) with increasing shell thickness (0-5.5 ML (monolayer)). We find that the shift of the LO2 peak from 268 to 291 cm(-1) agrees well with the theoretical values based on the phonon confinement model. The variation of the dielectric environment of the CdSe core with increasing CdS shell thickness is modified according to the shift of SO1 from 198 to 185 cm(-1). The SO2 modes at 267 and 275 cm(-1), corresponding to the shell thickness 3.5 and 5.5 ML in CdSe/CdS nanocrystals, respectively, are also obtained for the first time in our experiment. Moreover, they agree well with the theoretical values of the dielectric corresponding function model. Besides, a new Raman peak at 482 cm(-1) is observed, and it remains at that value with shell growth, the new peak is supposed to be caused by the alloying at the core-shell interface. Therefore, Raman spectroscopy can be used to determine the shell thickness and other surface and interface parameters of CdSe/CdS core-shell nanocrystals.

Serum HER2 as a predictive biomarker for tissue HER2 status and prognosis in patients with gastric cancer.

AIM: To investigate the association between serum human epidermal growth factor receptor 2 (HER2) extracellular domain (ECD) and tissue HER2 status, and the prognostic value of serum HER2 ECD in patients with gastric cancer. METHODS: A total of 239 patients with gastric cancer were enrolled from December 2012 to June 2013. Serum HER2 ECD was determined by chemiluminescent assay, and tissue HER2 status was evaluated by immunohistochemistry and fluorescence in situ hybridization assay. A receiver operating characteristic (ROC) curve was plotted to identify the optimal cut-off value for serum HER2 ECD assay for predicting survival in gastric cancer patients. RESULTS: Serum HER2 ECD was significantly correlated with tissue HER2 status (P < 0.001), tumor size (P < 0.001), and intestinal type of gastric cancer (P = 0.021). Serum HER2 ECD levels differed significantly between patients with HER2-positive tissue expression and those with HER2-negative tissue expression. ROC analysis yielded an area under the curve value of 0.79 (95%CI: 0.71-0.87, P < 0.001), with a sensitivity and specificity of 0.54 (95%CI: 0.37-0.70) and 0.93 (95%CI: 0.88-0.96), respectively. With a cut-off value of 24.75 ng/mL, high serum HER2 ECD had a negative impact on overall survival of the patients (HR: 1.93, 95%CI: 1.32-4.38, P = 0.006). CONCLUSION: Serum HER2 ECD could be a highly specific surrogate biomarker for tissue HER2 status in gastric cancer. Optimal cut-off criteria for predicting survival should be established.

[The effect of rosuvastatin therapy on CCR2 expression in mononuclear cells and its upstream pathway].

OBJECTIVE: To investigate the effect of rosuvastatin therapy on C-C chemokine receptor(CCR2)expression in mononuclear cells in patients with carotid atherosclerosis and explore the possible upstream mechanism. METHODS: Twenty patients without previous statin treatment were enrolled. Rosuvastatin were given 5 to 20 mg/day for 3 months. At baseline and 12 weeks, lipid profile and plasma monocyte chemotactic protein-1 (MCP-1) levels were examined. The mRNA and protein expressions of CCR2 in the mononuclear cells were measured with RT-PCR and flow cytometry, respectively. The mRNA and protein expression of peroxidase proliferator-activated receptor(PPAR ß) were detected with RT-PCR and Western blot, respectively. RESULTS: After 3-months rosuvastatin treatment, the patients' low-density lipoprotein cholesterol (LDL-C) levels decreased significantly (P<0.01). Compared with baseline, the mRNA and protein expressions of CCR2 in the mononuclear cells showed significantly decrease, as well as plasma MCP-1 levels (P<0.05). Both mRNA and protein expressions of PPAR ß in the mononuclear cells increased (P<0.05). CONCLUSIONS: Rosuvastatin may attenuate MCP-1/CCR2 through PPARß upstream pathway.

IL-17A stimulates the progression of giant cell tumors of bone.

PURPOSE: Giant cell tumors of bone (GCTB) exhibit aggressive bone lytic behavior. Studies have shown that interleukin 17A (IL-17A) is involved pathologic bone resorption in various skeletal disorders. Thus, we have investigated the role of IL-17A in GCTBs. EXPERIMENTAL DESIGN: We evaluated the progression of GCTBs using Campanacci grading and Enneking staging systems in 74 patients with GCTB. The expression of IL-17A and the IL-17A receptor A (IL-17RA) was assessed in GCTB tissues and in both multinucleated giant cells (MNGC) and stromal cells cultured in vitro using immunostaining and reverse transcription PCR (RT-PCR). The effects of IL-17A on the osteolytic activity of the MNGCs and the proliferation of the stromal cells were investigated using the "pit" formation and MTT assays, respectively. The effects of IL-17A on the expression of proosteolytic factors were examined in primary cultured MNGCs and stromal cells using RT-PCR, Western blotting, and gene expression microarrays. RESULTS: In GCTBs, we detected abundant levels of IL-17A, which were associated with tumor extension and grade. IL-17A is predominantly produced by MNGCs, whereas IL-17RA is expressed by both MNGCs and stromal cells in GCTBs. In the MNGCs, the IL-17A increased the mRNA expression of IL-17A and proosteolytic enzymes, and also enhanced osteolytic ability. In the stromal cells, the IL-17A stimulated cellular proliferation and the expression of proosteolytic factors, including RANKL through myc and STAT3, respectively. In addition, IL-17A stimulated in vivo tumor growth and the extent of angiogenesis in GCTBs. CONCLUSION: IL-17A stimulates the progression of GCTBs and might represent a useful candidate marker for progression and as a therapeutic target for GCTBs.