CXCL12 G801A polymorphism and susceptibility to glioma: a case­control study.

Previous studies have demonstrated that the CXCL12 G801A polymorphism is closely correlated with tumor susceptibility. In addition, the CXCL12/CXCR4 pathway is closely related to proliferation, metastasis, and invasion of glioma. However, the genetic effects of the CXCL12 G801A polymorphism on glioma risk in Chinese populations remain unknown. In this study, we investigated the potential associations between the CXCL12 G801A polymorphism with glioma susceptibility and its clinicopathological characteristics. Frequencies of CXCL12 G801A polymorphic variants between glioma patients (N = 750) and healthy controls (N = 750) were assessed using restriction length fragment polymorphism analysis. The association among the CXCL12 G801A polymorphism, glioma grade (WHO classification), and histological type was also evaluated. Our results showed that patients with glioma had significantly higher frequency of the CXCL12-3' A/A genotypes (P = 0.039) as compared with healthy controls. When stratified by the glioma histology, high-grade glioma patients had significantly higher frequency of the CXCL12-3' A/A genotypes (P = 0.019) as compared with low-grade glioma patients. When stratified by the WHO grade, significantly higher frequency of the CXCL12-3' A/A genotype was observed in stage IV glioma patients (P = 0.037). We conclude that the CXCL12 G801A polymorphism is a risk factor that increases susceptibility to gliomas in a subset of the general Han Chinese population.

Enhancement of focusing energy of ultra-thin planar lens through plasmonic resonance and coupling.

A metal-insulator-metal (MIM) structure which is used to enhance the focusing energy of planar lens is developed in this work. The top of the MIM structure is formed by circularly arranged V-shaped nanoantennas whose double resonance effect makes it possible for light to obtain great phase changes within an ultra-thin area. The middle and bottom of the structure is medium and gold film layer respectively. This structure produces plasmonic coupling between the antenna layer and gold film, thus reducing Ohmic loss and enhancing the effect of plasmonic excitation. When the distance between the antenna layer with a thickness of 30 nm and gold film is 88 nm, and the thickness of gold film is 20 nm, the enhancement of plasmonic coupling reaches to the strongest when the focusing intensity is 1.33 times higher than the lens only. With the advantages of small size, ultra-thin, great phase changes and high-efficient focusing ability, the enhanced plasmonic coupling lens structure can be widely applied in photoetching, and integrated optics.

Scanning and transmission electron microscopic studies on isolated ruptures of chordae tendineae.

Electron microscopic studies of chordae tendineae of the mitral valve were carried out in 17 patients who underwent mitral valve replacement due to a spontaneously isolated rupture of chordae tendineae. The normal chordae, used as the control group, were obtained at autopsy from 5 patients who died from extracardiac causes and were compared with the ruptured chordae. In all patients with chordal rupture, scanning electron microscopy showed perforations of the chordae tendineae, with extensive desquamation and disruption of the endothelial cells and wide-spread destruction of the collagen fiber bundles in the central collagenous core. These pathological findings were not observed in the normal chordae from the control group. Transmission electron microscopy showed that the ruptured chordae were characterized by heterogeneous collagen fibrils with intrinsic structural alterations and disorganization in fibril arrangement. There was a wide variation in the diameters of collagen fibrils which always showed abnormal morphology, with abnormally large, peculiarly shaped fibrils. Apparent loss and/or a disordered arrangement of the typical periodicity of the fibrils were frequently observed. In addition, various degrees of degenerative changes of collagen tissue were often present. These abnormalities were never seen in the fibrils of the normal chordae, and were observed consistently in both the fibrils of the ruptured chordae and in the macroscopically intact chordae in the group with spontaneous rupture of chordae tendineae. These results suggest that a defective organization of collagen into fibrils and fibers, associated with secondary degeneration of collagen within the central collagenous core of the chordae tendineae, are important pathogenetic mechanisms for spontaneously isolated ruptures of chordae tendineae.