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Biomedical subjects

K Thompson

Publications and source records attributed to K Thompson.

At least 235 records · Page 13Linked to original sources
PubMed1970

Effects of chronic excess salt ingestion. Inheritance of hypertension in the rat.

TWO STRAINS OF RAT HAVE BEEN DEVELOPED BY SELECTIVE BREEDING: one strain (R rats) is resistant to salt hypertension, the other strain (S rats) is highly susceptible. The inheritance of these traits has been explored in the first (F(1)) and second (F(2)) generation of crossbred rats and in backcrosses between parent and first filial (F(1) x R, F(1) x S) generations. Male F(1) rats had an average blood pressure close to the mid-parental (R and S) values, and the average of F(2) males was equivalent to that of F(1). Male offspring of F(1) with R, or F(1) with S also showed averages close to the respective mid-parental values. Female offspring showed deviations from this linear relationship, indicating a significant dominance in the female for the genes of normal blood pressure. A model of two autosomal, nonlinked diallelic loci, with a dominance deviation at one locus in the female, gave predictions with a reasonable agreement to the observed values. The same model also appeared compatible with human data if we assume a gene frequency of 0.13 for the hypertensinogenic allele on both loci. Random fluctuations in blood pressure, and incomplete homogeneity of parental strains permit several alternative models. The major conclusions are: that more than one locus is needed to explain the findings though as few as two loci may possibly suffice; the allelic effect seems additive in males, but there is a sex-determined influence on the expression in females; there is no consistent evidence for sex-linked inheritance. Furthermore, this model developed from the study of rats may provide a framework for analysis of human data.

Analysis of Variance↗
PubMedDate not supplied

Congenital sacrococcygeal teratomas: effect of gestational age on size, morphologic pattern, ploidy, p53, and ret expression.

Prognosis of infants born with sacrococcygeal teratomas (SCTs) correlates with gestational age (GA). The survival rate after 30 weeks of gestation is 75%, compared to 7% before 30 weeks of gestation. Studies correlating GA with size, morphologic composition of teratomas, ploidy or expression of cell cycle control proteins such as p53, and ret [a tyrosine kinase receptor of the GDNF (glial cell line-derived neurotrophic factors)] receptor family may provide information explaining differences in survival. Seven SCTs (GA 21 to 41 weeks), ranging in size from 5 to 15 cm, were evaluated for morphologic composition. DNA ploidy was assessed in mature and immature neural elements. Immunohistochemical reactivity with monoclonal antibodies recognizing p53, and ret was quantitated and correlated with morphological pattern and GA. Relative size of teratomas to infants' weight and content of immature neural tissues correlated inversely with advancement of GA. Yolk sac tumor (YST) and immature tissues showed aneuploid cell populations. Nuclear p53 reactivity was apparent in the teratoma with YST in the microcystic patterns, the neuroectodermal rosettes, and the glandular patterns. Ret reactivity was seen in osteoclasts adjacent to bone formation surrounding developing teeth in an immature teratoma, and in rare mature neural cells of one SCT of 35 weeks GA. The rapid growth of SCT (GA <30 weeks) correlates with increase in immature neural tissues. Our study confirms aneuploidy in YST and suggests aneuploid populations within immature tissues. p53 accumulates in a variety of patterns of YST and may be seen in immature components of SCTs. To understand the possible role of ret, further studies comparing ret expression in immature human tissues are needed.

Aneuploidy↗
PubMedDate not supplied

Increased cognitive sensitivity to scopolamine with age and a perspective on the scopolamine model.

18 older normal volunteers (mean age = 66.5 +/- 7.9 years) and 46 younger volunteers (mean age = 27.0 +/- 6.1 years) were administered the anticholinergic drug scopolamine (0.5 mg i.v.) followed by a battery of cognitive tests evaluating attention, learning and memory. The older subjects were significantly more impaired than the younger by scopolamine on some tests of learning and memory. This increased sensitivity of the older group to scopolamine is consistent with studies in animals and humans showing decreased cholinergic system function with age. The findings also indicate that age is an important variable to consider in using the scopolamine model of memory impairment. The cognitive impairment caused by scopolamine in younger subjects in this and prior studies is similar to some, but not all aspects of the impairment which occurs in normal aging. Scopolamine also caused impairments on digit span and word fluency tasks, which are not consistent with normal aging changes. In the older group of subjects, scopolamine produced aspects of the cognitive impairment which occurs in AD on tests of episodic memory and learning, vigilance-attention, category retrieval, digit span, and number of intrusions. Other areas of cognition that are of relevance to aging and AD such as psychomotor speed, praxis, concept formation and remote memory were not evaluated in this study. Some of these are being evaluated in ongoing studies, along with additional and more specific tests of retrieval from knowledge memory, implicit memory and attention. The scopolamine model has provided a fruitful pharmacologic starting point for the study of a number of cognitive operations. The idea of dissecting apart aspects of memory systems pharmacologically depends on the availability of neurochemically specific drugs and on the specificity and sensitivity of neuropsychological tests for distinct cognitive operations or domains. Further studies using such tools will aid not only in the understanding of the impairments which occur in aging and in AD, but also of the conceptualization of memory and other cognitive operations and ultimately the physiological mechanisms involved in memory and learning.

Acetylcholine↗
PubMedDate not supplied

Pediatric patients with bleeding dyscrasias: what is the cause of delays in initiating replacement therapy?

INTRODUCTION: The objectives of this study were to (a) evaluate the emergency department management of pediatric patients with bleeding disorders, specifically regarding time intervals from triage to administration of replacement therapy, and (b) to review resultant patient outcomes. METHODS: A retrospective review was performed of charts from June 1996 to June 1998 for all patients with known bleeding disorders whose course was followed by the hematology clinic. Records were reviewed for all emergency department visits that required replacement therapy. Time intervals from triage to initiation of therapy were evaluated. RESULTS: Eleven of 24 patients required administration of factor or desmopressin acetate. The mean time from triage to therapy administration was 103 minutes (range, 7 to 175 minutes; SD +/- 38). The mean time from triage to placement in a room was 34.3 minutes (SD +/- 32.6). The mean time to order replacement therapy was 26.7 minutes (SD +/- 27.4). The mean time from physician evaluation to administration of replacement therapy was 34.2 minutes (SD +/- 15.9). These intervals were believed to be suboptimal, and a new nursing driven protocol was established to expedite patient care. DISCUSSION: Simple delays in time to replacement therapy may result in increased patient morbidity. We present an easy-to-follow algorithm that can be implemented to expedite the care of pediatric patients with a known bleeding disorder.

Algorithms↗