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Family Tree (family + tree)

Distribution by Scientific Domains

Medical Sciences	33%
Life Sciences	33%

Selected Abstracts

The Biological Path to Reunification

GERMAN RESEARCH, Issue 2-3 2002
William Martin Prof.
The familiar form of the family tree is not applicable to all living organisms. Evolutionary history entails not only the divergence of lineages, but also mergers of distinct unicellular organisms (prokaryotes and protists) to form new cell types [source]

The Mathematical Assessment of Long-Range Linguistic Relationships

LINGUISTICS & LANGUAGE COMPASS (ELECTRONIC), Issue 5 2008
Brett Kessler
Language classification differs from biological cladistics in that monogenesis cannot be assumed. Before a cladogram or family tree can be accepted, linguists must be convinced that the languages are related at all. Morpheme tables, or word lists, provide a good framework for investigating relatedness, but methodologies for quantifying and assessing the data statistically are still being developed. The comparative method furnished a viable statistic, recurrent sound correspondences, but by no means to see whether they exceeded levels expected by chance. Organizing correspondences into contingency tables permitted hypothesis testing, with Monte Carlo resampling methods providing the flexibility to support a wide variety of test statistics, including different ways of computing sound recurrences and phonetic similarity. Thus, techniques from both the comparative method and multilateral comparison can be deployed with rigorous numeric assessment. Experiments seek to increase the power of the tests to explore new hypotheses and verify long-range language relationships. [source]

A Spectrum of Models of Signaling Pathways

CHEMBIOCHEM, Issue 10 2004
Sharat J. Vayttaden
How ready is biology for systems biology? This review surveys some 250 models and supporting experiments to assess how well major signaling pathways have been quantified. The review traces the family tree of MAPK models to show how modeling can evolve and has influenced the field. [source]

Aplasia cutis congenita, congenital heart lesions, and frontonasal cysts in four successive generations

CLINICAL GENETICS, Issue 6 2007
RG Rodrigues
We report a family with four known generations of individuals in the maternal family tree with aplasia cutis congenita (ACC) of the scalp, congenital heart lesions, brachydactyly, and frontonasal cysts. This is the first reported finding of craniofacial, digital, and cardiac abnormalities associated with ACC, likely representing a new variant of the autosomal dominant hidrotic ectodermal dysplasia subtype. These rare disorders are characterized by common anomalies of at least two elements of the ectoderm and its appendages, namely the skin, teeth, hair, nails, and sweat glands. These patients also frequently have chronic dental problems with early loss of teeth, and recurrent lung, ear, and nose infections secondary to a defect in mucous membrane function. The clinical findings in these patients are delineated and compared to patients with other forms of ectodermal dysplasia in the literature. [source]

Non-atopic intrinsic asthma and the ,family tree' of chronic respiratory disease syndromes

CLINICAL & EXPERIMENTAL ALLERGY, Issue 6 2009
P. G. Holt
Summary We present a scheme below in which the most common forms of inflammatory diseases of the respiratory tract, notably atopic and non-atopic asthma and COPD, are depicted as separate offshoots from a common ,at-risk' pathway underpinned by genotypes related to aberrations in control of host defence and tissue repair mechanisms. We propose that entrance into this pathway is initially programmed by environmental experience during infancy and early childhood, in particular by severe lower respiratory tract infection, and that further progression towards expression of specific disease phenotype(s) is determined by the nature, timing and frequency of additional environmental insults subsequently encountered. At the one extreme, early sensitization of at-risk subjects to aeroallergens can potentially drive rapid progression towards expression of the atopic asthmatic phenotype under the dual onslaught of inflammatory responses to allergens/pathogens. At the opposite end of the spectrum the drip-feed effects of occasional infections on respiratory function(s) are amplified over a longer time frame by inflammation resulting from exposure to tobacco smoke and/or related chemical pollutants. Non-atopic asthma is envisaged to fit between these two extremes, being driven essentially by the downstream effects of respiratory infections alone in at-risk subjects. An important common factor in all three disease phenotypes is that acute exacerbations are typically driven by infections, the host responses to which display a characteristic T-helper type 2-like footprint, which in our view points to underlying genotype(s) which result in unbalanced host responses to respiratory pathogens. [source]

Identification of Muir,Torre syndrome among patients with sebaceous tumors and keratoacanthomas

CANCER, Issue 5 2005
Role of clinical features, immunohistochemistry, microsatellite instability
Abstract BACKGROUND The Muir,Torre syndrome (MTS) is an autosomal-dominant genodermatosis characterized by the presence of sebaceous gland tumors, with or without keratoacanthomas, associated with visceral malignancies. A subset of patients with MTS is considered a variant of the hereditary nonpolyposis colorectal carcinoma, which is caused by mutations in mismatch-repair genes. The objective of the current study was to evaluate whether a combined clinical, immunohistochemical, and biomolecular approach could be useful for the identification of Muir,Torre syndrome among patients with a diagnosis of sebaceous tumors and keratoacanthomas. METHODS The authors collected sebaceous skin lesions and keratoacanthomas recorded in the files of the Pathology Department of the University of Modena during the period 1986,2000. Through interviews and examination of clinical charts, family trees were drawn for 120 patients who were affected by these skin lesions. RESULTS Seven patients also were affected by gastrointestinal tumors, thus meeting the clinical criteria for the diagnosis of MTS. In the MTS families, a wide phenotypic variability was evident, both in the spectrum of visceral tumors and in the type of skin lesions. Microsatellite instability was found in five MTS patients: These patients showed concordance with immunohistochemical analysis; moreover, a constitutional mutation in the MSH2 gene was found in 1 patient. Lack of expression of MSH2/MSH6 or MLH1 proteins was evident in the skin lesions and in the associated internal malignancies of 3 patients and 2 patients with MTS, respectively. CONCLUSIONS The clinical, biomolecular, and immunohistochemical characterization of sebaceous skin lesions and keratoacanthomas may be used as screening for the identification of families at risk of MTS, a disease that is difficult to recognize and diagnose. Cancer 2005. © 2005 American Cancer Society. [source]