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Morphological Stages (morphological + stage)

Distribution by Scientific Domains

Medical Sciences	50%

Selected Abstracts

Human telomerase catalytic subunit gene re-expression is an early event in oral carcinogenesis

HISTOPATHOLOGY, Issue 1 2004
B Luzar
Aims:, Detection of telomerase catalytic subunit (hTERT) mRNA has been used as a surrogate marker for estimation of telomerase activity. The exact role and timing of telomerase re-activation, a key enzyme implicated in cellular immortalization and transformation, in the multistep process of oral carcinogenesis is still unknown. The aim was to test the hypothesis that (i) quantitative rather than qualitative differences exist in the level of hTERT mRNA expression between normal oral mucosa, different grades of oral epithelial abnormalities and squamous cell carcinomas of the oral cavity, and that (ii) hTERT gene re-expression is an important, probably early event in oral carcinogenesis. Methods and results: The relative quantity of hTERT mRNA was analysed in 45 frozen oral epithelia representing different morphological stages of oral carcinogenesis classified according to the Ljubljana classification and in 37 oral squamous cell carcinomas, using a commercially available LightCycler Telo TAGGG hTERT Quantification kit. hTERT mRNA was not detected in normal or reactive hyperplastic oral epithelia, but was present in 43% of atypical hyperplasias (premalignant lesions), 60% of intraepithelial carcinomas and 68% of oral squamous cell carcinomas. Statistical analysis revealed two groups of oral epithelial changes, with significant differences in the levels of hTERT mRNA expression: 1, normal and reactive hyperplastic oral epithelium, and 2, atypical hyperplasia, intraepithelial carcinomas and squamous cell carcinomas. Conclusion:, These data suggest that hTERT gene re-expression represents an early event in the multistep process of oral carcinogenesis, already detectable at the stage of precancerous oral epithelial changes. Nevertheless, other genetic aberrations appear to be necessary for progression of oral epithelial abnormalities towards invasive squamous cell carcinoma. [source]

Effect of the stage of growth, wilting and inoculation in field pea (Pisum sativum L.) silages.

JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE, Issue 9 2006

Abstract The stage of growth, field wilting and inoculation with lactic acid bacteria (LAB) effects were studied by ensiling herbage of field pea (Pisum sativum L.) at four consecutive stages. Stands of semi-leafless field pea, sown in spring, were harvested at four progressive morphological stages (end of flowering, I; beginning of pod filling, II; advanced pod filling, III; beginning of ripening, IV). For each stage of growth, the herbage was field wilted to a dry matter (DM) content of 318, 300, 348 and 360 g kg,1 for stages I, II, III and IV, respectively. The unwilted and wilted herbages were ensiled in 5-L silos, with (I) and without (C) a LAB inoculant (Lactobacillus plantarum). High levels of ethanol, lactic acid and volatile fatty acids (VFA) were observed in all silages, facilitated by the high levels of water-soluble carbohydrates (WSC) at ensiling (from 111 to 198 g kg,1 DM). Despite the low pH values (4.3 and 4.1 for C and I silages, respectively), all the silages showed detectable levels of butyric acid. Field peas can be successfully ensiled after a short wilting period with reduced field curing and reduce DM losses onward from advanced pod filling stage, with the aid of LAB inoculum. Copyright © 2006 Society of Chemical Industry [source]

CPCR1, but not its interacting transcription factor AcFKH1, controls fungal arthrospore formation in Acremonium chrysogenum

MOLECULAR MICROBIOLOGY, Issue 5 2005
Birgit Hoff
Summary Fungal morphogenesis and secondary metabolism are frequently associated; however, the molecular determinants connecting both processes remain largely undefined. Here we demonstrate that CPCR1 (cephalosporin C regulator 1 from Acremonium chrysogenum), a member of the winged helix/regulator factor X (RFX) transcription factor family that regulates cephalosporin C biosynthesis, also controls morphological development in the ,-lactam producer A. chrysogenum. The use of a disruption strain, multicopy strains as well as several recombinant control strains revealed that CPCR1 is required for hyphal fragmentation, and thus the formation of arthrospores. In a ,cpcR1 disruption strain that exhibits only hyphal growth, the wild-type cpcR1 gene was able to restore arthrospore formation; a phenomenon not observed for ,cpcR1 derivatives or non-related genes. The intracellular expression of cpcR1, and control genes (pcbC, egfp) was determined by in vivo monitoring of fluorescent protein fusions. Further, the role of the forkhead transcription factor AcFKH1, which directly interacts with CPCR1, was studied by generating an Acfkh1 knockout strain. In contrast to CPCR1, AcFKH1 is not directly involved in the fragmentation of hyphae. Instead, the presence of AcFKH1 seems to be necessary for CPCR1 function in A. chrysogenum morphogenesis, as overexpression of a functional cpcR1 gene in a ,Acfkh1 background has no effect on arthrospore formation. Moreover, strains lacking Acfkh1 exhibit defects in cell separation, indicating an involvement of the forkhead transcription factor in mycelial growth of A. chrysogenum. Our data offer the potential to control fungal growth in biotechnical processes that require defined morphological stages for optimal production yields. [source]

Grading gastrointestinal dysplasia and what to call it when you don't know what it is,

THE JOURNAL OF PATHOLOGY, Issue 2 2007
GJ Offerhaus
Abstract Dysplasia in the gastrointestinal tract is defined as intraepithelial neoplasia (IEN) according to the WHO nomenclature. Neoplastic growth in the gastrointestinal tract evolves through stepwise tumour progression in which consecutive morphological stages are characterized by increasing genetic instability accompanied by specific genetic alterations. Invasive cancer is preceded by non-invasive precursor stages and the clonal epithelial cell proliferation in these pre-invasive stages is diagnosed as dysplasia or IEN. Dysplasia is therefore a marker for cancer risk and guides surveillance. Dysplasia is conventionally graded using a two-tier system and low- and high-grade dysplasia convey different connotations regarding cancer risk. This perspective argues that the critical differential diagnosis is the one between neoplastic and non-neoplastic epithelial cell proliferations and the relevance of grading dysplasia is questionable. It is furthermore expected that a molecular signature will predict the propensity to invasive carcinoma more accurately than routine histopathology in the near future. Research in this field needs to focus on a combination of biomarkers representing genetic instability, clonal mutations, and genetic clonal divergence. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source]