The morphology and mechanical properties of epoxy nanocomposites based on synthetic α-zirconium phosphate (α-ZrP) layer structure have been investigated. The interlayer surfaces of α-ZrP can be ...easily modified because of its high surface ion exchange capacity characteristics. The α-ZrP structure is layered claylike and possesses aspect ratios of at least 100. The state of exfoliation has been confirmed using direct transmission electron microscopy observation at various locations of the sample. With an addition of only 1.9 vol % α-ZrP, the tensile modulus of the α-ZrP-reinforced epoxy nanocomposite is increased by 50%, and the yield strength improved by 10%. However, the ductility of the matrix (elongation at break) is drastically reduced after the α-ZrP reinforcement. The fundamental structure−property relationship of α-ZrP-based epoxy nanocomposite is discussed.
Mammalian cytosolic glutathione S-transferases (GSTs; EC 2.5.1.18) form a supergene family consisting of four distinct families, named alpha, mu, pi and theta. In humans one member of the mu class ...gene family (GSTM1) has been shown to be polymorphic and is only expressed in 55-60% of individuals. Previous studies have shown a possible link with the null phenotype and susceptibility to cancer, in particular to lung cancer. In this study we genotyped individuals with breast, bladder and colorectal cancer. A total of 490 individuals with cancer were studied, and consisted of 97 bladder, 197 breast and 196 colorectal cancers. No significant differences were observed in the frequency of nulled individuals in bladder or breast cancer patients when compared with a control population of 225 individuals. However, a significant excess of nulled individuals were seen in colorectal cancer: 56.1% compared with the control group value of 41.8%. This was shown to be highly significant depending on the site of the tumours and > 70% of individuals with a tumour in the proximal colon were GSTM1 nulled. This is an approximately 2-fold increase in colon cancer risk in these individuals.
We report that mutation in the gene for plectin, a cytoskeleton-membrane anchorage protein, is a cause of autosomal recessive muscular dystrophy associated with skin blistering (epidermolysis bullosa ...simplex). The evidence comes from absence of plectin by antibody staining in affected individuals from four families, supportive genetic analysis (localization of the human plectin gene to chromosome 8q24.13-qter and evidence for disease segregation with markers in this region) and finally the identification of a homozygous frameshift mutation detected in plectin cDNA. Absence of the large multifunctional cytoskeleton protein plectin can simultaneously account for structural failure in both muscle and skin.
Background: We have previously demonstrated that breast cancers associated with inherited BRCA1 and BRCA2 gene mutations differ from each other in their histopathologic appearances and that each of ...these types differs from breast cancers in patients unselected for family history (i.e., sporadic cancers). We have now conducted a more detailed examination of cytologic and architectural features of these tumors. Methods: Specimens of tumor tissue (5-µm-thick sections) were examined independently by two pathologists, who were unaware of the case or control subject status, for the presence of cell mitosis, lymphocytic infiltration, continuous pushing margins, and solid sheets of cancer cells; cell nuclei, cell nucleoli, cell necrosis, and cell borders were also evaluated. The resulting data were combined with previously available information on tumor type and tumor grade and further evaluated by multifactorial analysis. All statistical tests are two-sided. Results: Cancers associated with BRCA1 mutations exhibited higher mitotic counts (P = .001), a greater proportion of the tumor with a continuous pushing margin (P<.0001), and more lymphocytic infiltration (P = .002) than sporadic (i.e., control) cancers. Cancers associated with BRCA2 mutations exhibited a higher score for tubule formation (fewer tubules) (P = .0002), a higher proportion of the tumor perimeter with a continuous pushing margin (P<.0001), and a lower mitotic count (P = .003) than control cancers. Conclusions: Our study has identified key features of the histologic phenotypes of breast cancers in carriers of mutant BRCA1 and BRCA2 genes. This information may improve the classification of breast cancers in individuals with a family history of the disease and may ultimately aid in the clinical management of patients. J Natl Cancer Inst 1998;90:1138–45
The chromosomal region 10q23-24 is frequently deleted in a number of tumour types, including prostate adenocarcinoma and glioma. A candidate tumour-suppressor gene at 10q23.3, designated PTENor ...MMAC1, with putative actin-binding and tyrosine phosphatase domains has recently been described. Mutations in PTEN have been identified in cell lines derived from gliomas, melanomas and prostate tumours and from a number of tumour specimens derived from glial, breast, endometrial and kidney tissue. Germline mutations in PTEN appear to be responsible for Cowden disease. We identified five PTEN mutations in 37 primary prostatic tumours analysed and found that 70% of tumours showed loss or alteration of at least one PTEN allele, supporting the evidence for PTEN involvement in prostate tumour progression. We raised antisera to a peptide from PTEN and showed that reactivity occurs in numerous small cytoplasmic organelles and that the protein is commonly expressed in a variety of cell types. Northern blot analysis revealed multiple RNA species; some arise as a result of alternative polyadenylation sites, but others may be due to alternative splicing.
One of the mantras of scientists working in the field of pharmacogenetics is ‘the right dose for the right patient’. A recent article has gone someway towards demonstrating that this goal can be ...achieved using genetic approaches. It is one of the first reports to show that a specific polymorphism can predict the maximum tolerated dose of two anti-epileptic drugs. However, further studies are necessary to validate these observations.
We have assembled a first-generation anchor map of the mouse genome using a panel of 94 whole-genome-radiation hybrids (WG-RHs) and 271 sequence-tagged sites (STSs). This is the first genome-wide RH ...anchor map of a model organism. All of the STSs have been previously localized on the genetic map and are located 8.8 Mb apart on average. This mouse WG-RH panel, known as T31, has an average retention frequency of 27.6% and an estimated potential resolution of 145 kb, making it a powerful resource for efficient large-scale expressed sequence tag mapping. All of the mapping data for the maps presented here have been deposited at the Research Genetics, Inc., web site and can be freely accessed and downloaded at http://www.resgen.com/.
The development of detailed single nucleotide polymorphism (SNP) maps of the human genome coupled with high-throughput genotyping technologies may allow us to unravel complex genetic traits, such as ...multifactorial disease or drug response, over the next few years. Here we describe the current efforts to identify and characterize the large numbers of SNPs required and discuss the practicalities of association studies for the identification of genes involved in complex traits.
Loss of the chromosomal region 10q23-25 is a frequent event in the progression of prostate adenocarcinoma. A candidate tumor suppressor gene from this region, Mxi1 at 10q25, has recently been shown ...to be mutated in a small number of prostate tumors. To more strictly define those regions of 10q loss that are likely to be involved in tumor advancement, we have constructed a detailed deletion map spanning 10q23-25 that incorporates Mxi1. Sixty-two % (23 of 37) of tumors analyzed exhibited some degree of 10q23-25 loss. Our data suggest the presence of a prostate tumor suppressor gene(s) near the 10q23-24 boundary, which was deleted in the overwhelming majority (22 of 23) of tumors showing loss. In contrast, specific loss of Mxi1, as opposed to loss of other 10q23-25 regions or of the entire region, was observed in only 1 of 23 tumors and was accompanied by loss of markers at the 10q23-24 boundary. Furthermore, we failed to detect any mutations in Mxi1 in those tumors showing Mxi1-associated marker loss by either single-strand conformation polymorphism analysis or direct DNA sequencing.
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