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Biomedical subjects

R M Porter

Publications and source records attributed to R M Porter.

14 recordsLinked to original sources
PubMed1996

Gene targeting at the mouse cytokeratin 10 locus: severe skin fragility and changes of cytokeratin expression in the epidermis.

Bullous congenital ichthyosiform erythroderma (BCIE) is a dominantly inherited blistering skin disorder caused by point mutations in the suprabasal cytokeratins 1 or 10. Targeting the murine cytokeratin 10 gene in ES cells resulted in mice with different phenotypes in the homozygotes and heterozygotes; both of which exhibit similarities to specific clinical characteristics of BCIE. Homozygotes suffered from severe skin fragility and died shortly after birth. Heterozygotes were apparently unaffected at birth, but developed hyperkeratosis with age. In both genotypes, aggregation of cytokeratin intermediate filaments, changes in cytokeratin expression, and alterations in the program of epidermal differentiation were observed. In addition we demonstrate, for the first time, the existence of the murine equivalent of human cytokeratin 16.

Animals↗
PubMed1993

Monoclonal antibodies to cytoskeletal proteins: an immunohistochemical investigation of human colon cancer.

Monoclonal antibodies raised to a number of microfilament-associated proteins were shown to recognize the appropriate proteins in extracts from human colon tissue. They were then used in an immunohistochemical study of normal colonic mucosa, adenomas, and adenocarcinomas. A strong reaction was seen in stromal cells within the tumours (both adenomas and adenocarcinomas) when frozen sections were stained with antibodies to filamin and caldesmon. In addition, a similar reaction was seen in the adenocarcinomas when stained with antibodies to talin and gelsolin. We believe that immunohistochemical staining with these antibodies reveals a tumour-induced process in the surrounding cells, possibly related to a host response to tumours.

Adenocarcinoma↗
PubMed1990

The influence of contralateral disease on the natural history of nonoperated significant carotid stenosis.

The influence of contralateral disease on the natural history of ipsilateral nonoperated carotid stenosis greater than 50% was analyzed in 90 carotid arteries imaged by contrast arteriography or duplex scanning with a mean follow-up of 23.6 months. Ipsilateral stenosis was greater than 80% in 24 arteries and 50-79% in 66 arteries. Contralateral disease was present in 30 (Group I) and absent in 60 (Group II) patients. In Group I, the contralateral disease consisted of total occlusion in nine (30%), greater than 80% stenosis in five (17%), 50-79% stenosis in 12 (40%) with a mean of 78.6%. No significant difference existed in the incidence of initially asymptomatic vessels (57% versus 67%), stroke (13% versus 2%), or transient ischemic attack (17% each) between Groups I and II on the ipsilateral side (p greater than .05). New ipsilateral neurologic events occurred significantly more often in arteries with greater than 80% ipsilateral stenosis than those with 50-79% stenosis (p less than .02). The incidence of subsequent ipsilateral neurologic events (37% versus 22%), strokes, or transient ischemic attacks (20% versus 13%) was no different in Groups I and II, respectively (p greater than .05). Combined ipsilateral and contralateral neurologic events occurred significantly more often in patients with contralateral disease (p less than .05). Whereas in Group I, new ipsilateral symptoms were significantly more common in initially symptomatic vessels compared to asymptomatic ones (61.5% versus 17.6%, p less than .04), no such difference existed in Group II.

Aged↗
PubMed1988

Natural history of nonoperated, significant carotid stenosis.

One-hundred sixty-seven patients with 190 carotid arteries (109 asymptomatic) demonstrating 50-99% stenosis by arteriography (80), duplex scanning, or other noninvasive techniques were followed from 1-84 months (mean 24.2) for evidence of brain infarct, transient ischemic attacks, or vertebrobasilar symptoms. Thirty-nine arteries (20.5%) were symptomatic at last follow-up, including 13 (6.8%) producing ipsilateral strokes. Twenty-eight sides underwent carotid endarterectomy, 16 for symptomatic lesions at a mean interval of 14.5 months after the initial diagnostic study, with no neurologic deficit. Twenty-seven patients (16.2%) died, eight from stroke (30%), and 12 from cardiac causes (44%). In initially symptomatic sides, the incidence of any subsequent neurologic event (28.7%) or stroke/transient ischemic attack (25%) was significantly greater than in asymptomatic arteries (14.6% and 12%, respectively) (p less than .05). Carotid arteries with greater than 80% stenosis by arteriography and duplex scanning had a 46% incidence of further symptoms and 41.6% stroke/transient ischemic attack rate compared to 19.6% and 15%, respectively, in arteries with less than 80% stenosis (p less than .01). Cumulative life table analysis at 12, 24 and 36 months showed greater than 80% stenosed arteries to have stroke/transient ischemic attack free rates of 69%, 50.5%, and 21.6% compared to 91%, 83.7%, and 76% for arteries with less than 80% stenosis (p less than .05). At a mean follow-up of over two years, nonoperated carotid stenosis (greater than 50%) carries a 20.5% risk of neurologic symptoms and a 6.8% risk of stroke, 61.5% of strokes being fatal. Symptomatic carotid stenosis had a significantly greater incidence of ensuing neurologic events than asymptomatic arteries.(ABSTRACT TRUNCATED AT 250 WORDS)

Arterial Occlusive Diseases↗
PubMed1974

Patient assessment.

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Antitubercular Agents↗