Improvement of piezoresistance properties of silicon carbide ceramics through co-doping of aluminum nitride and nitrogen

The piezoresistance coefficient was measured on co-doped silicon carbide ceramics. Evaluation samples of alpha-silicon carbide ceramics were first fabricated by glass capsule HIP method using powder mixture of silicon carbide and aluminum nitride with various ratios. The resultant aluminum nitride added silicon carbide ceramics were doped with nitrogen by changing the post-HIP nitrogen gas pressure. The lattice parameter increased with the amount of adding aluminum nitride indicating that the incorporated aluminum substituted smaller silicon atoms. After post-HIP treatment, lattice parameter then decreased with nitrogen gas pressure. The piezoresistive coefficient increased with the addition of aluminum nitride, it further increased with the nitrogen doping pressure

LAMC2 promotes gemcitabine resistance in PDAC

Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease with poor prognosis. Gemcitabine remains an effective option for the majority of PDAC patients. Unfortunately, currently no reliable prognostic and predictive biomarkers of therapeutic response are available for the patients with PDAC. Laminin γ2 (LAMC2) is overexpressed in several cancers, and its high expression facilitates cancer development and chemoresistance. However, its functional role in PDAC remains unclear, and a better understanding of this will likely help improve the prognosis of PDAC patients. This study aimed to elucidate the clinical and biological role of LAMC2 in PDAC. We first analyzed the expression levels of LAMC2 by real-time reverse transcription PCR in a cohort of 114 PDAC patients. Interestingly, higher expression of LAMC2 significantly correlated with poor survival in PDAC cohort. In addition, elevated LAMC2 expression served as a potential prognostic marker for survival. Subsequently, functional characterization for the role of LAMC2 in PDAC was performed by small interfering RNA (siRNA) knockdown in pancreatic cancer (PC) cell lines. Interestingly, inhibition of LAMC2 in PC cells enhanced the gemcitabine sensitivity and induction of apoptosis. Moreover, it inhibited colony formation ability, migration, and invasion potential. Furthermore, LAMC2 regulated the expression of epithelial-mesenchymal transition (EMT) phenotype. In addition, LAMC2 significantly correlated with genes associated with the expression of ATP-binding cassette (ABC) transporters in PC cells and PDAC patients. In conclusion, these results suggest that LAMC2 regulates gemcitabine sensitivity through EMT and ABC transporters in PDAC and may be a novel therapeutic target in PDAC patients

Identifying vertebral fractures in the Japanese population using the trabecular bone score : a cross-sectional study

Background: The trabecular bone score (TBS) is reported to be an independent predictor of fracture risk in patients with primary or secondary osteoporosis. However, there have been few reports on its use in the Japanese population. This study aimed to investigate the risk factors for vertebral fracture in the Japanese population and to evaluate the usefulness of TBS. Methods: This cross-sectional study involved 279 patients aged 60–90 years in whom bone mineral density (BMD) was measured by dual-energy X-ray absorptiometry (DXA). TBS was calculated based on the DXA scans. The presence or absence of vertebral fractures was assessed from T11 to L5. The patients were divided into those with vertebral fractures (VF group, n = 104) and those without vertebral fractures (non-VF group, n = 175). Results: Of the 104 patients in the VF group, 75 had 1 vertebral fracture and 29 had 2 or more fractures. The mean TBS was 1.28 in the VF group and 1.35 in the non-VF group (p  1.23). Conclusion: TBS was a significant indicator of vertebral fractures in the Japanese population and might contribute to identifying patients with vertebral fractures, particularly those with osteopenia who need pharmacologic therapy

Spatial re-organization of myogenic regulatory sequences temporally controls gene expression

During skeletal muscle differentiation, the activation of some tissue-specific genes occurs immediately while others are delayed. The molecular basis controlling temporal gene regulation is poorly understood. We show that the regulatory sequences, but not other regions of genes expressed at late times of myogenesis, are in close physical proximity in differentiating embryonic tissue and in differentiating culture cells, despite these genes being located on different chromosomes. Formation of these inter-chromosomal interactions requires the lineage-determinant MyoD and functional Brg1, the ATPase subunit of SWI/SNF chromatin remodeling enzymes. Ectopic expression of myogenin and a specific Mef2 isoform induced myogenic differentiation without activating endogenous MyoD expression. Under these conditions, the regulatory sequences of late gene loci were not in close proximity, and these genes were prematurely activated. The data indicate that the spatial organization of late genes contributes to temporal regulation of myogenic transcription by restricting late gene expression during the early stages of myogenesis. The Author(s) 2015. Published by Oxford University Press on behalf of Nucleic Acids Research

Macrophage centripetal migration drives spontaneous healing process after spinal cord injury.

Traumatic spinal cord injury (SCI) brings numerous inflammatory cells, including macrophages, from the circulating blood to lesions, but pathophysiological impact resulting from spatiotemporal dynamics of macrophages is unknown. Here, we show that macrophages centripetally migrate toward the lesion epicenter after infiltrating into the wide range of spinal cord, depending on the gradient of chemoattractant C5a. However, macrophages lacking interferon regulatory factor 8 (IRF8) cannot migrate toward the epicenter and remain widely scattered in the injured cord with profound axonal loss and little remyelination, resulting in a poor functional outcome after SCI. Time-lapse imaging and P2X/YRs blockade revealed that macrophage migration via IRF8 was caused by purinergic receptors involved in the C5a-directed migration. Conversely, pharmacological promotion of IRF8 activation facilitated macrophage centripetal movement, thereby improving the SCI recovery. Our findings reveal the importance of macrophage centripetal migration via IRF8, providing a novel therapeutic target for central nervous system injury