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N Barnard

Publications and source records attributed to N Barnard.

14 recordsLinked to original sources
PubMed1998

Development of a magnocellular function in good and poor primary school-age readers.

BACKGROUND: Abnormal functioning of the transient visual pathway (the M-pathway) has been implicated in specific reading disability (SRD). The aim of this study is to examine the contrast thresholds for flicker-defined form discrimination in primary school children, and to compare its development with reading and mentation development as a means of identifying children at risk of SRD. METHODS: One hundred eighty-seven children (aged 4 to 13 years) and 22 adults (aged 18 to 45 years) were assessed for contrast sensitivity to an illusory, flicker contrast-defined form (the letter 'E')--a task which was designed to rely to a large extent on magnocellular pathway function. Reading age (Neale Analysis of Reading) and mental age (Raven's Coloured Progressive Matrices) were assessed in the children, who had been previously screened for clinically normal binocular vision and refractive anomalies. RESULTS: The ability of primary school-age children to discriminate the orientation of the low contrast flickered letters (from a choice of 4) showed a significant improvement from kindergarten (ages 4 to 6 years) to grade 3 (ages 8 to 10 years) and older age groups. No significant difference was found between good and disabled readers (at least 1-year lag in reading readiness for the kindergarten group and 2-year lag in reading performance for 8 to 10 and 10 to 12-year-olds). CONCLUSIONS: It appears that there is a developmental improvement in perceptual capacity for tasks attributed to magnocellular function, which plateaus at the age of about 8 to 10 years. However, despite the reported reduction of magnocellular function in specific reading disabled children, no significant difference in contrast threshold for flicker-defined letter discrimination was found between good and poor readers.

Adolescent↗
PubMed1997

Dairy products and breast cancer: the IGF-I, estrogen, and bGH hypothesis.

Research on the role of dietary factors in breast cancer causation has focused predominantly on fat intake. While some studies have examined associations between breast cancer rates and consumption of whole milk, there has been less attention given to dairy products in general. Dairy products contain both hormones and growth factors, in addition to fat and various chemical contaminants, that have been implicated in the proliferation of human breast cancer cells. This literature review evaluates the epidemiological and mechanistic evidence linking dairy consumption with breast cancer risk.

Animals↗
PubMed1993

Epstein's syndrome. Implications for oral surgery.

Epstein's syndrome is a rare inherited disorder that appears principally as nephritis and deafness with thrombocytopathic thrombocytopenia producing a bleeding tendency. Management of the disorder for oral surgical procedures is discussed and highlighted by a case report.

Adult↗
PubMed1992

Endosseous implants in the irradiated composite radial forearm free flap.

This paper describes the application of endosseous titanium implants that have been inserted into the vascularized bone of the radial forearm composite flap, used for mandibular reconstruction. The technique described allows full orofacial rehabilitation to be achieved, following ablative surgery and adjuvant radiotherapy.

Bone Transplantation↗
PubMed1987

Interactions between cyclosporin A, indomethacin and 16,16-dimethyl prostaglandin E2: effects on renal, hepatic and gastrointestinal toxicity in the rat.

Rats were treated for 3 or 14 days with cyclosporin A (CsA, 50 mg/kg) or indomethacin (2 or 5 mg/kg) either alone or in combination, or with CsA plus 16,16-dimethylprostaglandin E2 (DMPGE2, 0.25 mg/kg). Hepatic and renal function were unaffected by treatment with indomethacin at either dose and only at the higher dose was severe intestinal ulceration observed. CsA caused renal and hepatic toxicity, evidenced by increased urine N-acetyl-beta-D-glucosaminidase activity, serum urea, creatinine and bilirubin and decreased serum albumin and total protein. In rats cotreated with CsA and either dose of indomethacin the increases in serum urea and creatinine and decreases in serum albumin and total protein were accentuated, but serum bilirubin was not further increased. Intestinal lesions were present in rats treated for 14 days with CsA plus the lower dose of indomethacin, but not in rats treated with either drug alone. In rats treated with DMPGE2 plus CsA, serum urea and creatinine were normal and urine N-acetyl-beta-D-glucosaminidase activity was reduced compared to rats treated with CsA alone, but DMPGE2 cotreatment had no effect on the CsA induced hyperbilirubinaemia. Hepatic microsomal cytochrome P-450 concentration and aminopyrine N-demethylase activity were lower in rats treated with CsA plus indomethacin than in untreated rats or those treated with either drug alone. Coadministration of indomethacin or DMPGE2 had no effect on serum trough CsA levels. The results are interpreted as showing an exacerbation by CsA of the intestinal toxicity of indomethacin, an increase by indomethacin in the renal toxicity of CsA and a protection by DMPGE2 against CsA renal toxicity. Possible mechanisms involving drug interactions and either hepatic cytochrome P-450, renal cyclooxygenase or other renal sites are discussed.

16,16-Dimethylprostaglandin E2↗
PubMedDate not supplied

AIDS presenting as mania.

Explore the source record for details and available documents.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

The inverse relationship between microvessel counts and tumor volume in breast cancer.

Angiogenesis has emerged as an indicator of metastatic potential in invasive breast cancer. Exponential tumor growth and the appearance of metastasis are observed as new microvessels form. We postulated that the relevance of angiogenesis would be enhanced if analyzed as a function of tumor volume rather than greatest diameter alone and that microvessel counts would proportionately increase as does volume. Since tumors are three-dimensional solids, volume was calculated using the formula for an ellipsoid, V = pi/6 (a x b x c). Sixty-four tumors < or = 2.5 cm were studied and analyzed in 5 mm incremental ranges. Mean microvessel counts did not vary significantly among these tumor size groups. However, analysis of microvessel counts as a function of tumor volume decreased from 947.1/cm3 (0-0.5 cm) to 18.1/cm3 (2.1-2.5 cm), a greater than 50-fold difference. High microvessel density in small cancers supports the notion of metastasis as an early event, making these small tumors perhaps ideal targets for antiangiogenic agents.

Breast Neoplasms↗