Enhancing the Oxidation Resistance of Al2O3-SiC-C Castables via Introducing Micronized Andalusite.

Additions of andalusite aggregates (19 wt%) were shown in previous literature to enhance the antioxidation of Al2O3-SiC-C (ASC) castables. This work aims to investigate whether micronized andalusite has a greater influence on antioxidation improvement than andalusite aggregates. Various low contents (5 wt% and below) of micronized andalusite (≤5 µm) were introduced as a substitute for brown fused alumina in the matrix of ASC castables. The antioxidation of castable specimens was estimated by the oxidized area ratio on the fracture surface after a thermal shock test. The microstructure and phases of micronized andalusite and the castable specimens were characterized by scanning electron microscopy (SEM) and X-ray diffraction (XRD), respectively. The results suggest that the antioxidation effects of ASC castables with a low addition of micronized andalusite are effectively enhanced. The heat-induced transformation of andalusite produces SiO2-rich glass, favoring the sintering of the castable matrix and impeding oxygen diffusion into the castable's interior. Therefore, the castable antioxidation is enhanced without deteriorating the hot modulus of rupture.

Differential expression of the CCN family member WISP-1, WISP-2 and WISP-3 in human colorectal cancer and the prognostic implications.

The WISPs (Wnt-inducted secreted proteins, WISP-1, WISP-2 and WISP-3) are part of the CCN family. These molecules are known to play a diverse role in cells but their role in cancer cells remains controversial. We analysed the expression of the three WISP molecules at the mRNA and protein levels in a cohort of 94 human colorectal tumours and 80 normal colorectal tissues and correlated the results with the pathological features and clinical outcome of the patients. WISP-1 transcripts were found at higher levels in the tumour samples than in the normal tissue (p=0.0015); higher in patients with Dukes stage B and C compared to Dukes A (p=0.017 and p=0.024, respectively); higher in patients with moderately and poorly differentiated cancers compared to the well differentiated cancers (p=0.020 and p=0.076, respectively and p=0.0035 when combined); higher in node positive tumours compared with the node negative (p=0.11) and in the patients with higher TNM staging (TNM 2, 3 and 4 compared to TNM 1 p=0.037). WISP-2 showed the opposite pattern with lower levels of expression in cancer cells compared to normal (p=0.082). Although no significant differences were found within the cancer group when indices of a more aggressive tumour were compared to the normal tissue a significant reduction in expression was found (Dukes C p=0.044, poorly differentiated p=0.019, TNM 3 p=0.020 and node positive disease p=0.048). WISP-3 transcript levels showed no significant differences between groups. WISPs may play important but contrasting roles in colorectal cancer with WISP-1 appearing to act as a factor stimulating aggressiveness, WISP-2 as a tumour suppressor and WISP-3 having no definable beneficial or detrimental role.

The transcript expression and protein distribution pattern in human colorectal carcinoma reveal a pivotal role of COM-1/p8 as a tumour suppressor.

BACKGROUND AND AIMS: COM-1(P8) is thought to play a role in the formation of metastases. This appears from current evidence to be different in various types of solid tumours. We aimed to examine the role COM-1 played in the development of colorectal cancer. MATERIALS AND METHODS: The expression of COM-1 mRNA was examined using a quantitative polymerase chain reaction (PCR) technique together with immunohistochemistry to examine expression and distribution of the COM-1 protein in human colorectal carcinoma and matched normal colorectal mucosa. RESULTS: COM-1 was expressed in 22.8% of normal colorectal mucosa samples and the expression in these tissues was 54.9 copies of COM-1 transcript per sample. In tumour tissues, 43.6% of samples expressed COM-1, at a level of 98.9 copies of COM-1 transcript per sample (p=0.012). Normal tissues demonstrated strong nuclear and peri-nuclear staining for COM-1 on immunohistochemistry (IHC) and in tumour tissues, the level of staining was found to be much greater, with a greater degree of cytoplasmic staining and little nuclear staining. Early-stage tumours showed a greater degree of staining on IHC compared to those at an advanced stage of disease. CONCLUSION: COM-1, although overexpressed at the messenger level, appears to be distributed in a cytoplasmic fashion at the protein level in tumours. Tumours at advanced stage express COM-1 protein to a lesser extent than their early-stage counterparts.