Optimized Design of a Pump Laser System for a Spin Exchange Relaxation Free Inertial Measurement Device.

In order to improve the precision and beam quality of a pump laser for a spin exchange relaxation free inertial measurement device, we applied one scheme to achieve the square wave modulation and power stability control of the pump laser and another one to obtain the uniform intensity distribution of the laser beam, in which the acousto-optic modulator (AOM) and proportion integration differentiation (PID) controller were used to achieve the former, and the freeform surface lens was designed and optimized to achieve the latter based on the TracePro software. In experiments, the first-order diffraction light beam coming through the AOM had a spot size of about 1.1×0.7 mm2, and a spherical vapor cell with a radius of 7 mm was placed behind the freeform surface lens. Results show that the uniformity of the reshaped intensity distribution is higher than 90% within the target area with a radius of 7 mm both in the simulation and the experiment, which ensure that the uniform laser beam covers the area of cell. On the other hand, the power stability of the pump laser is controlled to be less than 0.05%. Compared with traditional methods, the complicated calculation process in optical design is better solved, and a higher uniformity with slight energy loss is achieved.

Arctigenin enhances the sensitivity of cisplatin resistant colorectal cancer cell by activating autophagy.

Arctigenin is the active content of arctium lappa that present anti-cancer abilities in various carcinomas. However, its role and underlying mechanism in drug-resistant colorectal cancer cells has not been addressed. The present study used SW480 and SW620 to established cisplatin-resistant colorectal cancer cell lines, and explored the impact of arctigenin on these cells. Arctigenin at 100 µM significantly inhibited cell proliferation of cisplatin treated R-SW480 and R-SW620 cells as compared with cells treated with cisplatin alone. Arctigenin elevates cell apoptosis, up-regulated pro-apoptotic protein cleaved-caspase-3 and caspase-9 expression level in cisplatin treated R-SW480 and R-SW620 cells. Additionally, arctigenin triggered autophagy and promoted LC3-Ⅱ and p65 expression, while inhibited LC3-Ⅰexpression. Arctigenin impeded the IC50 of not only cisplatin but also oxaliplatin, doxorubicin and Paclitaxel of R-SW480 and R-SW620 cells. More importantly, the mRNA expression of multi drug resistance 1 (MDR1) and protein expression of pgp were significantly inhibited by arctigenin administration. Taken together, arctigenin has the potential in sensitize colorectal cancer cells by activating autophagy, which induced cell apoptosis and inhibited cell growth. Our study revealed that arctigenin has the potential for colorectal cancer treatment and may be useful in adjuvant chemotherapy.

Glioma malignancy is linked to interdependent and inverse AMOG and L1 adhesion molecule expression.

BACKGROUND: Gliomas account for the majority of primary human brain tumors and remain a challenging neoplasm for cure due to limited therapeutic options. Cell adhesion molecules play pivotal roles in the growth and progression of glial tumors. Roles of the adhesion molecules on glia (AMOG) and L1CAM (L1) in glioma cells have been shown to correlate with tumorigenesis: Increased expression of L1 and decreased expression of AMOG correlate with degree of malignancy. METHODS: We evaluated the interdependence in expression of these molecules by investigating the role of AMOG in vitro via modulation of L1 expression and analyzing apoptosis and cell senescence of glioma cells. RESULTS: Immunohistochemical staining of normal human cortical and glioma tissue microarrays demonstrated that AMOG expression was lower in human gliomas compared to normal tissue and is inversely correlated with the degree of malignancy. Moreover, reduction of AMOG expression in human glioblastoma cells elevated L1 expression, which is accompanied by decreased cell apoptosis as well as senescence. CONCLUSION: AMOG and L1 interdependently regulate their expression levels not only in U-87 MG cells but also in U251 and SHG44 human glioma cell lines. The capacity of AMOG to reduce L1 expression suggests that methods for increasing AMOG expression may provide a therapeutic choice for the management of glial tumors with high expression of L1.

CHL1 Is Expressed and Functions as a Malignancy Promoter in Glioma Cells.

The cell adhesion molecule with homology to L1CAM (close homolog of L1) (CHL1) is a member of the cell adhesion molecule L1 (L1CAM) gene family. Although CHL1 expression and function have been reported in several tumors, the roles of CHL1 in the development of glioma remain unclear. In the present study, we investigated the effects of CHL1 on proliferation indexes and activation of Akt1 and Erk signaling by siRNA in U-87 MG human glioblastoma and human U251 and SHG-44 glioma cells. We found that siRNA targeting CHL1 significantly down-regulated the expression of CHL1 mRNA and protein accompanied by reduced cell proliferation and transmigration invasion in all three cell lines. Down-regulating CHL1 expression also reduced cell survival, as measured by the Bax/Bcl-2 ratio, and increased activation of caspase-3. In subcutaneous U-87 MG cell xenograft tumors in nude mice, intratumoral administration of siRNA targeting CHL1 treatment significantly down-regulated CHL1 expression in vivo, accompanied by increased levels of activated caspase-3. Our combined results confirmed for the first time that in contrast to findings about CHL1 in most other cancer types, CHL1 functions in promoting cell proliferation, metastasis and migration in human glioma cells both in vitro and in vivo. These results indicate that CHL1 is a therapeutic target in the clinical management of glioma/glioblastoma.

Differential changes in Neuregulin-1 signaling in major brain regions in a lipopolysaccharide-induced neuroinflammation mouse model.

Neuregulin 1 (Nrg1) is involved in multiple biological processes in the nervous system. The present study investigated changes in Nrg1 signaling in the major brain regions of mice subjected to lipopolysaccharide (LPS)-induced neuroinflammation. At 24 h post­intraperitoneal injection of LPS, mouse brain tissues, including tissues from the cortex, striatum, hippocampus and hypothalamus, were collected. Reverse transcription­polymerase chain reaction was used to determine the expression of Nrg1 and its receptors, Neu and ErbB4, at the mRNA level. Western blotting was performed to determine the levels of these proteins and the protein levels of phosphorylated extracellular signal-regulated kinases (Erk)1/2 and Akt1. Immunohistochemical staining was utilized to detect the levels of pNeu and pErbB4 in these regions. LPS successfully induced sites of neuroinflammation in these regions, in which changes in Nrg1, Neu and ErbB4 at the mRNA and protein levels were identified compared with controls. LPS induced a reduction in pNeu and pErbB4 in the striatum and hypothalamus, although marginally increased pErbB4 levels were found in the hippocampus. LPS increased the overall phosphorylation of Src but this effect was reduced in the hypothalamus. Moreover, increased phosphorylation of Akt1 was found in the striatum and hippocampus. These data suggest diverse roles for Nrg1 signaling in these regions during the process of neuroinflammation.