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Biomedical subjects

N Hopwood

Publications and source records attributed to N Hopwood.

8 recordsLinked to original sources
PubMed1999

"Giving body" to embryos. Modeling, mechanism, and the microtome in late nineteenth-century anatomy.

Reinvestigating the work of the anatomist Wilhelm His (1831-1904) shows how engaging with models in three dimensions can revise our accounts of scientific change. His is known to historians of biology for articulating a mechanical approach to embryology and for inventing a section cutter, or microtome. Focusing on the wax models that he also made in the late 1860s shows how the other two innovations were linked; reconstructing embryos from the sections, His claimed, provided compelling evidence for mechanical views. The next generation of embryologists appropriated His's work selectively. In the 1880s anatomists took up "plastic reconstruction" to visualize the complex forms of higher vertebrate, especially human, embryos. An increasingly dominant experimental embryology, by contrast, drew on His's mechanical approach but had little use for the waxes and effaced them from the history of his work. Recovering these models offers a fresh perspective on the transformation of a central science of animal life and enriches our understanding of the relations between representation in two dimensions and three.

Animals↗
PubMed1997

Partial growth-hormone insensitivity: the role of growth-hormone receptor mutations in idiopathic short stature.

Mutations in the GHR locus may play a role in the cause of idiopathic short stature (ISS) by impairing growth-hormone (GH) receptor (GHR) function. At one extreme, mutations that nullify the function of the GH receptor are linked to complete GH insensitivity syndrome, or Laron syndrome, and we hypothesized that less-disruptive mutations could contribute to partial GH insensitivity syndrome. Low levels of GH binding protein may indicate mutations in the extracellular domain of the receptor, and by focusing on 14 children with ISS who had low GH binding protein and insulin-like growth factor I levels, we found three heterozygotes and one compound heterozygote for mutations in the extracellular domain of the receptor. We have since extended our study to a broader spectrum of patients, adding 76 patients with ISS who were treated with GH in a phase II study of the safety and efficacy of recombinant human GH in ISS and also adding 10 patients who were ascertained as having ISS by pediatric endocrinologists in private practice. The GHR gene has thus been analyzed in 100 patients with ISS, eight of whom were found to carry mutations: four in our original study and four with normal or elevated levels of GH binding protein. The latter group consists of three carriers of heterozygous extracellular domain mutations and one carrier of a heterozygous intracellular domain mutation. Family data suggest that the carriers of these mutations have a range of phenotypes, supporting our hypothesis that the expression of these heterozygous mutations as partial GH insensitivity syndrome depends on the genetic makeup of the person.

Body Height↗
PubMed1991

Diagnostic significance of urinary growth hormone measurements in children with growth failure: correlation between serum and urine growth hormone.

Twelve-h overnight urine and serum samples obtained simultaneously at 20-min intervals were assayed for growth hormone (GH). Ninety-one children, 5 to 16 y (Tanner stage 1 to 3) participated; group 1 were healthy children, group 2 were children with organic GH deficiency, and group 3 had idiopathic growth failure and normal GH stimulation tests. Serum pool GH concentrations in group 1 were similar to those in group 3 (3.3 +/- 0.3 versus 3.4 +/- 0.2 micrograms/L); group 2 had significantly lower GH concentrations (1.6 +/- 0.2 micrograms/L). Plasma IGF-I levels were significantly greater in groups 1 (14.2 +/- 2.6 nmol/L, p less than 0.001) than in groups 2 and 3 (2.6 +/- 0.5 and 5.5 +/- 0.7 nmol/L, respectively). Urinary GH (mean +/- SEM) standardized for body weight (micrograms/kg) in group 1 (0.31 +/- 0.02) was significantly greater than in group 2 (0.14 +/- 0.01) and group 3 (0.20 +/- 0.01). However, when expressed as microgram/mol creatinine, the output of GH was similar in group 1 (4.0 +/- 0.3) and group 3 (3.4 +/- 0.3); both groups had significantly greater output compared to group 2 (1.3 +/- 0.2). Urinary IGF-I (nmol/kg) in group 1 (0.22 +/- 0.02) was significantly greater than in group 2 (0.12 +/- 0.01) or group 3 (0.07 +/- 0.01). Urinary GH correlated with serum pool GH concentration (r = 0.64, p less than 0.001). Although urinary GH output reflects endogenous GH secretion, the overlap between groups 1 and 3 precludes using urinary GH measurements as a diagnostic test for GH deficiency in children with idiopathic growth failure.

Adolescent↗
PubMed1979

[TSH-screening program for congenital hypothyroidism. Experiences with early thyrotropin (TSH) screening].

14,919 newborn infants were screened for congenital hypothyroidism within the last 5 years using a sensitive TSH method. 10 infants with congenital hypothyroidism were discovered thus presenting a frequency of 1:4500. Four of these infants showed abnormally high TSH levels and normal thyroxine levels. The determination of TSH in cord blood--or combined with the screening program for phenylketonuria--in eluate of dried filter paper specimens is the most sensitive test for primary hypothyroidism without false negative results and a low false positive recall rate of 0.16%. After initiation of therapy with thyroxine the TSH level falls unless therapy is delayed for longer. In the latter case TSH levels may remain elevated for several months despite therapy with thyroxine. We would suggest to start therapy with triiodothyronine for up to 14 days prior to initiation of the usual thyroxine therapy.

Congenital Hypothyroidism↗