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Biomedical subjects

D Barker

Publications and source records attributed to D Barker.

At least 73 records · Page 4Linked to original sources
PubMed1996

Evaluation of a food frequency questionnaire used to assess nutrient intakes in pregnant women.

OBJECTIVE: To compare nutrient intakes assessed by food frequency questionnaire (FFQ) with those determined from food diaries. DESIGN: A 100-item FFQ was administered to women at 15 weeks of pregnancy. Food diaries were kept for a 4-day period at 16 weeks of pregnancy. SETTING: Community-based study of a general population sample of pregnant women booked for delivery at the Princess Anne Maternity Hospital, Southampton, UK. SUBJECTS: 603 women were recruited. Complete dietary data were provided by 569 women. RESULTS: Nutrient intakes determined by FFQ were greater than those from food diaries. Spearman rank correlation coefficients for macronutrients ranged from 0.27 (protein and starch) to 0.37 (fat). Stronger correlations for energy, fat and carbohydrate were seen in women who did not experience nausea, suggesting that the level of agreement observed between the FFQ and food diary in the whole group may be an underestimate of the true agreement. The percentage of individuals classified to the same quarter of the distribution of nutrient intake by the FFQ and diaries ranged from 30% (starch) to 41% (calcium), with between 4% (riboflavin) and 8% (energy, protein and vitamin E) classified to the opposite quarters. Using serum vitamin C as an independent biomarker of intake, the percentage of individuals classified to the correct quarter of intake was similar for the FFQ and diary (34% and 37%), with 8% (FFQ) and 6% (diary) misclassified to the opposite quarter. CONCLUSION: The FFQ appears to give meaningful estimates of nutrient intake in early pregnancy which can be used to rank individuals within the distribution.

Adult↗
PubMed1996

DNA sequencing by capillary electrophoresis with a hydroxyethylcellulose sieving buffer.

Capillary electrophoresis (CE) is capable of rapid, high-resolution separations of DNA. The technique has been adopted for both ssDNA and dsDNA applications. In order to make CE more convenient and cost-effective, replaceable sieving buffers have recently been developed. For DNA sequencing, the most successful of these replaceable buffers have been carefully polymerized and purified viscous linear polyacrylamide solutions. However, the hazards of acrylamide are well documented, and the care required to prepare the appropriate molecular weight polymer make this approach less than ideal. We report use of a replaceable sieving buffer suitable for DNA sequencing by CE that is easy to prepare and uses commercially available, non-toxic hydroxyethylcellulose.

Buffers↗
PubMed1995

Comparison of the responses of human melanocytes with different melanin contents to ultraviolet B irradiation.

Melanin is thought to serve in photoprotection. To investigate this, we have compared the responses of cultured human melanocytes derived from different pigmentary phenotypes (skin types I-VI) to a single irradiation with different doses of UVB light, ranging between 11.7 and 70.1 mJ/cm2. After UVB irradiation, heavily pigmented melanocytes had the same percent survival but a greater capacity to resume proliferation than their lightly pigmented counterparts. A significant increase in melanin content was observed in heavily pigmented but not in lightly pigmented melanocytes. Irradiation with UVB light blocked melanocytes, regardless of their melanin content, in G1, and induced the expression of the tumor suppressor p53 protein within 4 h. This induction steadily increased up to 48 h in lightly pigmented melanocytes; however, in heavily pigmented melanocytes, p53 level peaked at 24 h after UVB treatment and declined thereafter. Additionally, DNA from lightly pigmented melanocytes contained significantly higher numbers of cyclobutane pyrimidine dimers than did DNA from heavily pigmented melanocytes after irradiation with increasing doses of UVB light. We speculate that the prolonged induction of p53 in lightly pigmented melanocytes arrests them in G1 for a long time period in order to repair extensive DNA damage. The above described differences might partially explain the increased susceptibility of individuals with lightly pigmented skin compared to individuals with dark skin to the photodamaging and photocarcinogenic effects of sun exposure.

Cell Cycle↗
PubMed1995

Childhood growth, physical activity, and peak bone mass in women.

Peak bone mass is an important determinant of the risk of osteoporotic fracture, and preventive strategies against osteoporosis require a clear understanding of the factors influencing bone gain in early life. We report a longitudinal study aiming to identify the relationships between childhood growth, lifestyle, and peak bone mass in women. One hundred and fifty-three women born in a British city during 1968-1969 were traced and studied in 1990. Data on their growth in childhood was obtained from linked birth and school health records; current bone mineral measurements were made by dual X-ray absorptiometry. There were statistically significant associations between weight at 1 year and BMC (but not BMD) at the lumbar spine (r = 0.32, p < 0.01) and femoral neck (r = 0.26, p < 0.01). These remained significant after adjusting for current weight. There were also strong relationships between childhood height measurements and adult BMC at the two skeletal sites. Physical activity was the major lifestyle determinant of BMD after allowing for body build. We conclude that infant growth and physical activity in childhood are important determinants of peak bone mass in women. Growth primarily determines the size of the skeletal envelope, and its trajectory is established by age 1 year. Activity, in contrast, modulates the mineral density within the skeletal envelope and may contribute to the consolidation of bone following the end of linear growth.

Absorptiometry, Photon↗
PubMed1995

A new X linked recessive deafness syndrome with blindness, dystonia, fractures, and mental deficiency is linked to Xq22.

X linked recessive deafness accounts for only 1.7% of all childhood deafness. Only a few of the at least 28 different X linked syndromes associated with hearing impairment have been characterised at the molecular level. In 1960, a large Norwegian family was reported with early onset progressive sensorineural deafness, which was indexed in McKusick as DFN-1, McKusick 304700. No associated symptoms were described at that time. This family has been restudied clinically. Extensive neurological, neurophysiological, neuroradiological, and biochemical, as well as molecular techniques, have been applied to characterise the X linked recessive syndrome. The family history and extensive characterisation of 16 affected males in five generations confirmed the X linked recessive inheritance and the postlingual progressive nature of the sensorineural deafness. Some obligate carrier females showed signs of minor neuropathy and mild hearing impairment. Restudy of the original DFN-1 family showed that the deafness is part of a progressive X linked recessive syndrome, which includes visual disability leading to cortical blindness, dystonia, fractures, and mental deficiency. Linkage analysis indicated that the gene was linked to locus DXS101 in Xq22 with a lod score of 5.37 (zero recombination). Based on lod-1 support interval of the multipoint analysis, the gene is located in a region spanning from 5 cM proximal to 3 cM distal to this locus. As the proteolipid protein gene (PLP) is within this region and mutations have been shown to be associated with non-classical PMD (Pelizaeus-Merzbacher disease), such as complex X linked hereditary spastic paraplegia, PLP may represent a candidate gene for this disorder. This family represents a new syndrome (Mohr-Tranebjaerg syndrome, MTS) and provides significant new information about a new X linked recessive sydromic type of deafness which was previously thought to be isolated deafness.

Adolescent↗
PubMed1995

Middle cerebral artery blood flow velocity and stable xenon-enhanced computed tomographic blood flow during balloon test occlusion of the internal carotid artery.

BACKGROUND AND PURPOSE: Transcranial Doppler ultrasonography has been reported to reflect changes in cerebral blood flow (CBF) with the use of radioactive tracer techniques, which are weighted to measure primarily cortical structures. We tested the hypothesis that changes in transcranial Doppler ultrasonography would reflect changes in CBF in the middle cerebral artery vascular territory with the use of stable xenon-enhanced CT to assess CBF during carotid occlusion. METHODS: Thirty-one conscious patients underwent balloon test occlusion of the internal carotid artery and transcranial Doppler ultrasonography and xenon-enhanced CT assessment of blood flow velocity and CBF, respectively, of the middle cerebral artery and its distribution during balloon test occlusion. RESULTS: A significant correlation was seen between the change in CBF and the change in blood flow velocity for both brain levels at which CBF was determined (P < .0001). The average change in blood flow velocity was -13.4%, and the change in CBF was -15.1% and -17.7% at the two anatomic levels examined. CONCLUSIONS: The data indicate that changes in blood flow velocity generally reflect changes in CBF throughout the middle cerebral artery vascular territory with abrupt occlusion of the internal carotid artery in unanesthetized humans.

Adult↗
PubMed1992

Charcot-Marie-Tooth neuropathy type 1A mutation: apparent crossovers with D17S122 are due to a duplication.

A locus for the slow conducting form of Charcot-Marie-Tooth neuropathy (CMT1A) was localised to the proximal short arm of chromosome 17, in band p11.2, distal to D17S58. Linkage studies of CMT1A in 3 large Australian families with the marker loci D17S58, D17S71, and D17S57 suggested the order, pter-CMT1A-D17S71-D17S58-centromere-D17S57. However, the estimate of the recombination fraction between CMT1A and D17S122, also assigned to p11.2, was incompatible with known map distances. The impasse was resolved when the D17S122 genotypes were revised to take into account a dosage effect due to a duplication. After correction of the genotypes, the maximum lod score between CMT1A and D17S122 increased from 0.53 at a recombination fraction of 0.3 to 34.28 at zero recombination. This result emphasizes that genotypes for markers in the p12-p11.2 region should be examined very carefully as ignoring the duplication changes the linkage results dramatically. The fact that no crossovers were found between CMT1A and D17S122 suggests that the duplication may cause the disease phenotype.

Charcot-Marie-Tooth Disease↗
PubMed1992

A study of glycogen depletion and the fibre-type composition of cat skeleto-fusimotor units.

1. We have used the glycogen-depletion technique, combined with myofibrillar ATPase (mATPase) staining for muscle fibre type, to study the fibre-type composition of four skeleto-fusimotor (beta) units in cat peroneus tertius, namely, one beta dynamic (beta d) unit and three beta static (beta s) units. 2. Depletion of glycogen was observed in serial cross-sections of thirty-four beta-unit extrafusal muscle fibres of various types traced from origin to insertion. No fibre was depleted of glycogen throughout its length; depletion was restricted to a number of zones, usually about five. Oxidative (type I) and oxidative-glycolytic (type IIA) fibres were depleted for a significantly greater proportion of their total length than glycolytic IIB fibres. 3. The fibre-type composition of the beta d unit was determined by tracing its fibres from end to end. The muscle unit consisted of one intrafusal bag1 fibre and ninety-three extrafusal muscle fibres comprising seventy-six type I fibres, eleven IIC fibres, and six fibres that changed from IIC to I during the course of their length (IIC/I fibres). The extrafusal fibre-type composition was thus 81.7% I plus 18.3% IIC and IIC/I. 4. The three beta s units (beta s1, beta s2, beta s3) were all fast-contracting and fatigued rapidly. Identification of their extrafusal fibre types, made in 1 mm2 areas sampled from different parts of each unit, gave mixed compositions as follows: beta s1, IIB + 6.7% IIA; beta s2, IIB + 5.8% IIA; beta s3, IIB + 29.9% IIA. The intrafusal component of each unit included either one or two long chain fibres. 5. In a discussion of the results, the fact that the continuous stimulation of extrafusal muscle fibres does not deplete them of glycogen throughout their length is examined in relation to the work of others who have assumed that it did. With regard to the finding of mixed extrafusal fibre types in the beta units, a distinction is drawn between minimal (around 5%) and moderate mixing. It is suggested that minimal mixing may occur in any motor unit as the outcome of endplate degeneration with foreign replacement, but that moderate mixing indicates an on-going process of conversion from one fibre type to another which in the adult may prove to occur only among beta units.

Animals↗
PubMed1992

An X-linked human collagen transgene escapes X inactivation in a subset of cells.

Transgenic mice carrying one complete copy of the human alpha 1(I) collagen gene on the X chromosome (HucII mice) were used to study the effect of X inactivation on transgene expression. By chromosomal in situ hybridization, the transgene was mapped to the D/E region close to the Xce locus, which is the controlling element. Quantitative RNA analyses indicated that transgene expression in homozygous and heterozygous females was about 125% and 62%, respectively, of the level found in hemizygous males. Also, females with Searle's translocation carrying the transgene on the inactive X chromosome (Xi) expressed about 18% transgene RNA when compared to hemizygous males. These results were consistent with the transgene being subject to but partially escaping from X inactivation. Two lines of evidence indicated that the transgene escaped X inactivation or was reactivated in a small subset of cells rather than being expressed at a lower level from the Xi in all cells, (i) None of nine single cell clones carrying the transgene on the Xi transcribed transgene RNA. In these clones the transgene was highly methylated in contrast to clones carrying the transgene on the Xa. (ii) In situ hybridization to RNA of cultured cells revealed that about 3% of uncloned cells with the transgene on the Xi expressed transgene RNA at a level comparable to that on the Xa. Our results indicate that the autosomal human collagen gene integrated on the mouse X chromosome is susceptible to X inactivation. Inactivation is, however, not complete as a subset of cells carrying the transgene on Xi expresses the transgene at a level comparable to that when carried on Xa.

Animals↗
PubMed1991

Localization of Charcot-Marie-Tooth disease type 1a (CMT1A) to chromosome 17p11.2.

Charcot-Marie-Tooth (CMT) disease type 1a has been previously localized to chromosome 17 using the markers D17S58 and D17S71. In that report we were unable to provide unequivocal localization of the CMT1A gene on either the proximal p or the q arm. Therefore, data from one additional CMT1A family and typing of other probes spanning the pericentromeric region of chromosome 17 (D17S73, D17S58, D17S122, D17S125, D17S124) were analyzed. Multipoint analysis demonstrates convincing evidence (log likelihood difference greater than 5) that the CMT1A gene lies within 17p11.2 and most likely between the flanking markers D17S122 and D17S124.

Charcot-Marie-Tooth Disease↗
PubMed1990

The achondroplasia gene is not linked to the locus for neurofibromatosis 1 on chromosome 17.

We have investigated genetic linkage of von Recklinghausen neurofibromatosis (NF1) and achondroplasia (ACH) using chromosome-17 markers that are known to be linked to NF1. Physical proximity of the two loci was suggested by the report of a patient with mental retardation and the de novo occurrence of both NF1 and ACH. Since the chance of de novo occurrence of these two disorders in one individual is 1 in 600 million, this suggested a chromosomal deletion as a single unifying molecular event and also that the ACH and NF1 loci might be physically close. To test this, we performed linkage analysis on a three-generation family with ACH. We used seven DNA probes that are tightly linked to the NF1 locus, including DNA sequences that are known to flank the NF1 locus on the centromeric and telomeric side. We detected two recombinants between the ACH trait and markers flanking the NF1 locus. In one recombinant, the flanking markers themselves were nonrecombinant. Multi-point linkage analysis excluded the ACH locus from a region surrounding the NF1 locus that spans more than 15 cM (lod score less than -2). Therefore, analysis of this ACH pedigree suggests that the ACH locus is not linked to the NF1 locus on chromosome 17.

Achondroplasia↗
PubMed1990

Glycoprotein C-dependent attachment of herpes simplex virus to susceptible cells leading to productive infection.

Herpes simplex viruses encode several glycoproteins dispensable for infection and replication in cell culture. Evidence is presented that there exist at least two pathways for viral attachment to cells, i.e., one mediated by the dispensable glycoprotein C (gC) and one independent of that glycoprotein. Thus, whereas the polycations neomycin and polylysine inhibit attachment but not entry of already attached herpes simplex virus 1 (HSV-1) into baby hamster kidney (BHK) cell line, they have no effect on HSV-2 attachment to the same cells (N. Langeland, H. Holmsen, G.R. Lilehaug, and L. Haarr, 1987, J. Virol. 61, 3388-3393; N. Langeland, L.J. Moore, H. Holmsen, and L. Haarr, 1988, J. Gen. Virol. 69, 1137-1145). We report that (i) analyses of intertypic HSV-1 X HSV-2 recombinants indicated that the HSV-2 locus which confers ability to infect BHK cells in the presence of neomycin or polylysine comaps with the gene specifying gC but not with or near the genes specifying the other viral glycoproteins (gB, gD, gE, and gG, and gI), (ii) the smallest HSV-2 DNA fragment capable of transferring this function to HSV-1 was a 2880-bp Sa/l fragment encoding the entire gC (UL44 open reading frame) gene, 515 bp of coding sequences from the UL43 open reading frame and 393 bp of coding sequences from the UL45 open reading frame, but analyses of the recombinant virus DNA excluded UL43 and most of the UL45 sequences, and (iii) definitive evidence that HSV-2 gC confers upon HSV the capacity to infect BHK cells in the presence neomycin or polylysine emerged from studies showing that site-specific mutagenesis which inactivated the gene yielded a recombinant whose attachment to BHK cells was blocked by the polycations. We conclude that in BHK cells there exists in addition to the pathway blocked by neomycina and polylysine a pathway which is parallel and HSV-2 gC dependent.

Animals↗
PubMed1990

Regeneration and recovery of cat muscle spindles after devascularization.

1. We have assessed the sensory reinnervation and recovery of regenerated muscle spindles in extensor digitorum longus (EDL) 6, 8 and 13 weeks after the muscle, with its nerve left intact, had been devascularized. Recordings were made from the dorsal roots of the responses of single afferent fibres to ramp-and-hold stretch of the regenerated spindles whose sensory reinnervation was subsequently examined in teased, silver preparations. 2. The spindle population in four normal EDL muscles ranged from 53 to 83 (mean 69); analysis of the afferent innervation of 166 normal b1b2c spindles showed that 23% had primary endings supplied by two Ia afferents. Regenerated spindles were identified as belonging to one of four groups in which afferents establish sensory endings on intrafusal muscle fibres in groups 1-3, but not in group 4. Sensory reinnervation was complete after 6 weeks recovery and similar proportions of group 1-3 spindles occurred after each recovery period, i.e. 58% after 6 weeks, 65% after 8 weeks and 62% after 13 weeks. We estimate that about half the original spindle population was lost owing to persistent ischaemic necrosis; that 30% regenerated and acquired functional afferent connections (group 1-3 spindles); and that the total loss of spindle afferents was over 60%. 3. The conduction velocities of the regenerated spindle afferents were very similar to those of normal EDL spindle afferents. The proportions that responded normally to ramp-and-hold stretch at the end of each recovery period increased from 58% after 6 weeks to 61% after 8 and 88% after 13. Other responsive spindle afferents were either predominantly phasic or only responded to supramaximal stretch. The proportions of these decreased as recovery progressed reducing from 19% after 6 weeks to 9% after 13 weeks in the case of those giving predominantly phasic responses and from 23% after 6 weeks to 3% after 13 weeks in the case of those unresponsive to physiological stretch. 4. The mean peak and held firing rates of regenerated spindle afferents responsive to 10 mms-1 ramp-and-hold stretches were all significantly lower than normal. There was no marked trend towards higher firing rates after longer periods of recovery through, considered separately, the mean peak firing rates of the normally responding afferents did show a distinct improvement. The mean dynamic and velocity indexes were not significantly different from normal. 5. The ratio of Ia:spindle II afferents, as identified by their responses to stretch, was 1:1.22 in the control animals and 1:1.26 in the experimental series.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗