The use of solution processes-as opposed to conventional vacuum processes and vapour-phase deposition-for the fabrication of electronic devices has received considerable attention for a wide range of applications, with a view to reducing processing costs. In particular, the ability to print semiconductor devices using liquid-phase materials could prove essential for some envisaged applications, such as large-area flexible displays. Recent research in this area has largely been focused on organic semiconductors, some of which have mobilities comparable to that of amorphous silicon (a-Si); but issues of reliability remain. Solution processing of metal chalcogenide semiconductors to fabricate stable and high-performance transistors has also been reported. This class of materials is being explored as a possible substitute for silicon, given the complex and expensive manufacturing processes required to fabricate devices from the latter. However, if high-quality silicon films could be prepared by a solution process, this situation might change drastically. Here we demonstrate the solution processing of silicon thin-film transistors (TFTs) using a silane-based liquid precursor. Using this precursor, we have prepared polycrystalline silicon (poly-Si) films by both spin-coating and ink-jet printing, from which we fabricate TFTs with mobilities of 108 cm2 V(-1) s(-1) and 6.5 cm2 V(-1) s(-1), respectively. Although the processing conditions have yet to be optimized, these mobilities are already greater than those that have been achieved in solution-processed organic TFTs, and they exceed those of a-Si TFTs (< or = 1 cm2 V(-1) s(-1)).

We have developed a liquid precursor that can be used in a solution process to form n-type doped silicon films. This precursor is based on phosphorus-doped hydrogenated polysilane synthesized by photo-copolymerizing cyclopentasilane and white phosphorus. By spin-coating this precursor, we have prepared n-type amorphous silicon films and polycrystalline silicon films with resistivities of 6.5–27 Ω·cm and 2.0–10 mΩ·cm, respectively.

Phosphorylated p38 (p-p38) played a pivotal role in the regulation of disease progression and correlated with tumor prognosis. Here, we characterized the prognostic effect of p-p38 in colorectal cancer (CRC). Three hundred and sixteen CRC patients in stages I-III were recruited in this study. P-p38 expression was semi-quantitatively evaluated using tissue microarrays and immunohistochemistry staining. Overall survival (OS), disease-free survival (DFS), local failure-free survival (LFFS), and distant metastasis-free survival (DMFS) of patient subgroups, segregated by p-p38 expression level and clinical stage, were compared using Kaplan-Meier analysis. We found that p-p38 was overexpressed in 48.1 % (152/316) CRC tissues, whereas low or deficiently expressed in normal adjacent epithelia. Overexpression of p-p38 predicted poor OS (P < 0.001), DFS (P = 0.002), LFFS (P = 0.016), and DMFS (P = 0.025) in CRC. Importantly, patient subgroups in the early stage (stages I + II) and with low p-p38 had similar OS, PFS, LFFS, and DMFS probabilities to that of stage I, whereas those with high p-p38 were similar to stage III disease. In addition, for stage III disease, the subgroup with low p-p38 had a similar survival probability to that of stage I, whereas the subgroup with high p-p38 had the worst survival. Multivariate Cox analysis confirmed that p-p38 was indeed a significantly independent factor for death, recurrence, and distant metastases in CRC. Our results demonstrated that p-p38 was a negative independent prognostic factor for CRC. Complementing TNM staging with p-p38 might refine the risk definition more accurately for a subset of patients.

Our results reveal an underlying mechanism of radiation-induced acute enteritis, which may help clarify the pathogenesis of RE and point to potential targets for therapeutic interventions.

Abstract. Mitogen-activated protein kinase kinase kinase 2 (MEKK2) is an important upstream mediator of the extracellular signal-regulated kinase 5 signaling cascade that is essential for a number of cellular functions, including mitogenesis, differentiation and oncogenic transformation. Using western blotting to examine MEKK2 expression in 16 cases of primary colorectal cancer (CRC) lesions with paired normal mucosa, it was identified that MEKK2 is highly expressed in CRC lesions compared with that of the normal mucosa. Immunohistochemistry of 24 normal mucosa, 24 adenoma and 96 adenocarcinoma colorectal specimens indicated that the expression of MEKK2 was significantly increased in the adenoma and carcinoma specimens compared with that of the normal mucosa cases (P<0.0001 for both). However, no significant differences were detected in MEKK2 expression between the carcinoma and adenoma specimens (P=0.85). Similarly, no correlations were identified between MEKK2 expression and clinicopathological features, including gender, age, body mass index, histological differentiation, depth of invasion, lymph node metastasis, UICC stage and K-ras mutations (P>0.05). The present study demonstrated that MEKK2 functions as a promotive factor in CRC. IntroductionColorectal cancer (CRC) is the second and third most common type of malignancy in females and males worldwide, respectively (1). In the majority of Asian countries, CRC morbidity has increased rapidly throughout previous decades, and follows a stepwise progression from normal tissue to a premalignant phase to the invasive carcinoma. This process is known as the adenoma-carcinoma sequence. Recently, a number of studies have suggested that the accumulation of multiple gene mutations in key signaling pathways correlates with the multiple steps of colorectal carcinogenesis (2,3). Therefore, it is essential to identify significant molecular biomarkers in these pathways for the prevention and treatment of CRC.Mitogen-activated protein kinase kinase kinase 2 (MEKK2) is a Ser/Thr protein kinase expressed in multiple tissues that belongs to the MEKK/STE11 subgroup of the MAP3K family (4,5). Specifically, MEKK2 is a member of the extracellular signal-regulated kinase 5 (ERK5) signaling cascade that has been previously identified in all four mitogen-activated protein kinase (MAPK) pathways, including MEKK2/3, MEK5 and ERK5 at the MAP3K, MAPKK and MAPK tiers, respectively (6). The ERK5 signaling cascade is essential for the control of cellular proliferation (7) and is likely to be targeted during cell cycle progression (8,9) and tumorigenesis (10,11). In addition, the ERK5 cascade is involved in the management of cell differentiation (12,13), migration (14,15), neuronal survival rate (16), embryonic angiogenesis (17) and additional cellular functions (18-21).MEKK2 has been shown to mediate epidermal growth factor and fibroblast growth factor 2 receptor signals (22,23) which have been previously identified to be involved in the development of various types of cancer (24,25). There...