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Biomedical subjects

R M Porter

Publications and source records attributed to R M Porter.

16 recordsLinked to original sources
PubMed1998

The relationship between hyperproliferation and epidermal thickening in a mouse model for BCIE.

Epidermal thickening is a phenomenon common to many genodermatoses but little is known about the underlying causes. We have recently created a mouse model for the human skin disease bullous congenital ichthyosiform erythroderma by gene targeting. Mice heterozygous for a truncated keratin 10 gene exhibit acanthosis and hyperkeratosis as seen in the human disease. The degree of epidermal thickening is highly variable, offering a novel opportunity to investigate how epidermal homeostasis is modulated in keratin disorders by comparing epidermis from different body regions. We have performed bromodeoxyuridine labeling experiments and detected proliferation antigens by immunohistochemical means to compare proliferation in the epidermis of wild-type and heterozygous mice. These results have been compared with the expression of epidermal differentiation markers and of the "hyperproliferation associated" keratins K6 and K16. These experiments indicated that hyperproliferation is only partly responsible for the morphologic changes and that other mechanisms such as decreased desquamation are likely to be involved.

Animals↗
PubMed1997

Therapeutic and protective efficacy of doramectin injectable against gastrointestinal nematodes in cattle in New Zealand: a comparison with moxidectin and ivermectin pour-on formulations.

Two similar studies were conducted in New Zealand to compare the therapeutic and persistent activity of doramectin injectable, moxidectin pour-on, ivermectin pour-on and oxfendazole oral drench when administered to nematode-infected cattle which were then grazed on common pastures. On day 0 (treatment day), 40 cattle were weighed, faecal sampled and allocated on the basis of day--3 faecal egg counts (FEC) to four treatment groups. Cattle were then treated with either doramectin by subcutaneous (s.c.) injection, moxidectin and ivermectin by topical application, or oxfendazole orally using label-recommended dosages. Oxfendazole treatment served primarily as a control to monitor reinfection without persistent activity. Faecal samples for nematode egg counts and coprocultures for larval differentiation were collected six times between day 0 and day 56 and all cattle were reweighed on day 56. Doramectin reduced pretreatment FEC by 99.1% in the first study and by 100% in the second study when assessed at 14 days posttreatment. Corresponding reductions for moxidectin were 80.8% and 85.2%, for ivermectin 86.0% and 80% and oxfendazole 78.3% and 100%, respectively. Posttreatment rise in FEC indicated that reinfection of moxidectin-treated animals occurred at the same time as oxfendazole controls in both trials. Posttreatment rise in FEC with ivermectin pour-on was similar to moxidectin and oxfendazole in one study, but in the other study ivermectin pour-on delayed the rise by 14-21 days. The rise in FEC for doramectin was delayed for 14-21 days in one study and at least 21 days in the other. The better parasite control provided by doramectin resulted in greater weight gains for cattle over the 56-day period as compared to moxidectin pour-on, ivermectin pour-on and oxfendazole in both trials. Gains of doramectin treated cattle were significantly (p < 0.05) greater than those of ivermectin and moxidectin groups in one trial and the oxfendazole group only in the other.

Administration, Oral↗
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↗