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Biomedical subjects

S J Ellis

Publications and source records attributed to S J Ellis.

At least 19 recordsLinked to original sources
PubMed1998

Is forced dextrality an explanation for the fall in the prevalence of sinistrality with age? A study in northern England.

OBJECTIVES: The fall in the prevalence of left handedness with age has been attributed to either premature mortality or a cohort effect of forced dextrality. Evidence for forced dextrality was sought to differentiate between these competing theories. DESIGN: 6097 Edinburgh handedness inventories were used to calculate laterality quotients (LQ) with and without the questions relating to writing and drawing. These questions might be expected to be most influenced by forced dextrality. SETTING: The study was performed in a small industrial town in Lancashire, UK. PARTICIPANTS: Using the British family practitioner service where over 95% of the population are registered with a general practitioner a response rate of 82.17% was obtained with respect to the Edinburgh Inventory. RESULTS: Questions about writing and drawing on the Edinburgh Inventory contributed to the positivity (right handedness) of the mean LQ, but equally across the ages. When a negative LQ was used to define left handedness the prevalence of left handedness fell from 11.2% at age 15 to 4.4% at age 70. Removal of the questions about writing and drawing caused the prevalence of left handedness to fall from 10.5% at age 15 to 4.95% at age 70. CONCLUSIONS: Less than 20% of the fall in the prevalence of left handedness was accounted for by questions relating to writing and drawing. The fall in the prevalence of sinistrals in older age groups is not adequately explained by cohort effects of forced dextrality on the writing hand.

Adolescent↗
PubMed1997

Tremor and other movement disorders after whiplash type injuries.

Movement disorders are usually of central origin, but have been reported in association with peripheral trauma. Injuries to the neck of the whiplash type provide a source of both types of injuries. Six cases are reported in which the temporal relation between the injury and the movement disorder make a causal relation likely. This important cause of disability has not previously been appreciated.

Adolescent↗
PubMed1997

Cloning and characterization of an uncoupling protein homolog: a potential molecular mediator of human thermogenesis.

We have identified a novel cDNA encoding a protein highly homologous to the mammalian brown fat uncoupling protein (UCP). Unlike the known UCP, which is expressed specifically in brown adipose tissue, the UCP homolog (UCPH) mRNA is expressed in a variety of tissues, with predominant expression in human white adipose tissue and skeletal muscle. In the white adipose tissue of ob/ob and db/db mice, the UCPH transcript is induced approximately fivefold relative to lean littermate controls. Expression of murine UCPH in yeast results in growth inhibition under conditions that require aerobic respiration, but does not affect growth under anaerobic conditions. Furthermore, UCPH expression in yeast causes a decrease in the mitochondrial membrane potential, as judged by staining with the potential-sensitive dye DiOC6. These observations suggest that UCPH, like UCP, uncouples oxidative phosphorylation. The possibility that the UCPH protein is an important mediator of human thermogenesis is discussed.

Amino Acid Sequence↗
PubMed1996

Evidence that the diabetes gene encodes the leptin receptor: identification of a mutation in the leptin receptor gene in db/db mice.

OB-R is a high affinity receptor for leptin, an important circulating signal for the regulation of body weight. We identified an alternatively spliced transcript that encodes a form of mouse OB-R with a long intracellular domain. db/db mice also produce this alternatively spliced transcript, but with a 106 nt insertion that prematurely terminates the intracellular domain. We further identified G --> T point mutation in the genomic OB-R sequence in db/db mice. This mutation generates a donor splice site that converts the 106 nt region to a novel exon retained in the OB-R transcript. We predict that the long intracellular domain form of OB-R is crucial for initiating intracellular signal transduction, and as a corollary, the inability to produce this form of OB-R leads to the severe obese phenotype found in db/db mice.

Alternative Splicing↗