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K Evans

Publications and source records attributed to K Evans.

At least 91 records · Page 5Linked to original sources
PubMed1995

A possible involvement of VIP in feeding-induced secretion of ACTH and corticosterone in the rat.

For decades it has been known that brain/gut peptides are released during the ingestion of a meal. Although a multitude of actions have been attributed to these peptides acting in the brain, including the release or inhibition of a variety of pituitary hormones, the actual physiological roles of these substances in the brain have not been confirmed. For the first time, we have demonstrated that feeding-induced hypothalamic-pituitary-adrenal (HPA) secretion may involve the brain/gut peptide, vasoactive intestinal peptide (VIP), acting in the paraventricular nucleus (PVN) of the hypothalamus. The effects of 24 h fasting and refeeding on the release of plasma ACTH and CORT secretion in male rats were investigated. Blood samples were collected 5 min prior to PVN administration of saline or VIP antagonist, [Lsy, Pro, Arg, Tyr]-VIP and 30 min after refeeding. Plasma ACTH and CORT concentrations were significantly increased by 43 and 485%, respectively, by 30 min ingestion of food. Pretreatment with the VIP antagonist (0.75 and 1.5 nmol/rat) significantly reduced the food-induced ACTH response by 69 and 76% and the CORT response by 58 and 65%, respectively. There were no significant differences in food-intake among groups. These results suggest that one potential role of hypothalamic VIP may involve activation of hypothalamic-releasing factors to regulate ACTH and CORT levels during or after a meal.

Adrenocorticotropic Hormone↗
PubMed1995

Puberty, sexual milestones and abuse: how are they related in eating disorder patients?

In order to assess the relationship pubertal development, sexual milestones and childhood sexual abuse in women with eating disorders, 44 patients with restricting anorexia nervosa (RAN), 26 with bulimic anorexia nervosa (BAN), 29 with bulimia nervosa and also with a history of anorexia nervosa (BN/HistAN), and 69 with bulimia nervosa but without a history of anorexia nervosa (BN) completed questionnaires on pubertal and sexual development and unpleasant sexual experiences. Forty-four female college students complete the sexual development questionnaire only. Different eating disorder groups were found to be similar in terms of their pubertal development. All eating disorder groups showed delays in aspects of their psychosexual development (age at first kiss, masturbation, genital fondling and first sexual intercourse) compared with the control group, although to a different degree. The RAN group was delayed on almost all sexual milestones whereas the other groups were delayed on only some. On some variables, most noticeably on first sexual intercourse, restricters also were more delayed than the other eating disorder groups. Similarly, the median number of sexual partners differed significantly between groups (RAN = 1, BAN = 2, BN/HistAN = 4, BN = 4, controls = 5, P < 0.0001). Eating disorder patients, in particular RAN patients, were less positive about sexual relationships than controls, but did not differ from controls in attitudes to masturbation, marriage, children or pregnancy. Of the eating disorder patients 22-31% had been sexually abused during childhood. A history of abuse affected attitudes to masturbation, but did not appear to affect sexual development.

Adolescent↗
PubMed1995

The role of molecular genetics in the prenatal diagnosis of retinal dystrophies.

Inherited retinal dystrophies are important causes of incurable blindness in developed countries. Advances in molecular genetics promise significant improvements in their management. Immediate benefits of present knowledge are presymptomatic and prenatal diagnosis in selected cases. To study the predictive power of these techniques a simulated genetic risk estimation was undertaken in a cone-rod retinal dystrophy pedigree known to be linked to chromosome 19. Using data on five fully informative, flanking DNA markers, phenotype was correctly assigned with only a 2% probability of error. If the two most closely linked markers were found to be uninformative, this error probability remained unchanged. Using genetic risk calculations and direct mutation detection many retinal dystrophies could now be identified by prenatal diagnosis.

Blindness↗
PubMed1995

Scattered radiation in a neonatal surgical unit.

We studied the doses of "scattered" received by neonates in a Neonatal Surgical Unit by placing thermoluminescent dosemeters in various positions expect the direct beam. Doses of "scattered" radiation received by neonates as a results of exposure of their neighbours to X-ray examinations were found to be negligible. Sick neonates need not be moved from their neighbours undergoing exposure to X-rays.

Humans↗
PubMed1995

Localization of the gene for progressive bifocal chorioretinal atrophy (PBCRA) to chromosome 6q.

Progressive bifocal chorioretinal atrophy (PBCRA) is a rare, autosomal dominant congenital chorioretinal dystrophy. We have performed genetic linkage analysis on a five-generation British pedigree. Two-point linkage analysis showed significant linkage with nine microsatellite marker loci mapping to chromosome 6q. Multipoint analysis gave a maximum lod score of 11.8 (theta = 0.05) between D6S249 and D6S283. This region overlaps with that to which the gene for North Carolina macular dystrophy (MCDR1) has been assigned. However, given the range of differences in phenotype between these two retinal disorders, it is likely that different mutation mechanisms are responsible for each disease.

Atrophy↗
PubMed1995

Absolute 99Tcm-DMSA renal uptake in children: optimum time to scan.

Absolute renal uptake was measured at 2, 4 and 6 h in 27 patients in order to determine a more convenient time for uptake compared with the 6-h measurement proposed by other authors. Measurements made at 2 and 4 h would need to be increased by 20 and 6%, respectively, to convert to the value at 6 h. Measurements at 4 h are a reasonable compromise to achieve a high-count/low-background image in a reasonable time and to obtain a good estimate of the predicted 6 h uptake at a single scanning session. The percent renal uptake at 6 h, U(6), can be derived from the percent uptake measured at t hours after injection, U(t), using the following formula: U(6) = U(t) x CF(t), where CF(t) = 1.0 + 0.03 (6 - t) for 4 < or = t < or = 6.

Adolescent↗
PubMed1995

Effect of the method of breast feeding on breast engorgement, mastitis and infantile colic.

This exploratory study compared the effect of two methods of breast feeding on breast engorgement, mastitis, infantile colic and duration of breast feeding. An opportunity sample of subjects was assigned either to the experimental group (prolonged emptying of one breast at each feed) (n = 150) or to the control group (both breasts equally drained at each feed) (n = 152) and both groups were followed prospectively to 6 months after delivery. The experimental group had a lower incidence of breast engorgement in the first week (61.4% versus 74.3%; p < 0.02) and colic over the first 6 months (12% versus 23.4%; p < 0.02). There was no significant difference between the two groups in the incidence of mastitis over 6 months and the length of breast feeding (16.5 +/- 10.3 weeks versus 17.5 +/- 10 weeks experimental versus control group). The majority of mothers in the experimental group (63%) felt it necessary to offer the second breast at the end of a feed to satisfy their infant's hunger. The "perceived insufficient milk supply syndrome" was the main reason given for cessation of breast feeding in both groups. This study provides data to advise nursing mothers about these two methods of breast feeding.

Adult↗
PubMed1995

Bimodal expressivity in dominant retinitis pigmentosa genetically linked to chromosome 19q.

A clinical, psychophysical, and electrophysiologic study was undertaken of two autosomal dominant retinitis pigmentosa pedigrees with a genetic mutation assigned to chromosome 19q by linkage analysis. Members with the abnormal haplotype were either symptomatic with adolescent onset nyctalopia, restricted visual fields, and non-detectable electroretinographic responses by 30 years of age, or asymptomatic with normal fundus appearance and minimal or no psychophysical or electroretinographic abnormalities. There was no correlation in the severity in parents and their offspring. Pedigree analysis suggested that although the offspring of parents with the genetic mutation were at 50% risk of having the genetic defect, the risk of being symptomatic during a working lifetime was only 31%. Such bimodal phenotypic expressivity in these particular pedigrees may be explained by a second, allelic genetic influence and may be a phenomenon unique to this genetic locus. Genetic counselling in families expressing this phenotype can only be based on haplotype analysis since clinical investigations, even in the most elderly, would not preclude the presence of the mutant gene.

Adult↗
PubMed1995

Genetic refinement of the chromosome 5q lattice corneal dystrophy type I locus to within a 2 cM interval.

Lattice corneal dystrophy type I (LCDI) is a relatively common corneal dystrophy which can cause severe visual impairment. Recent studies have suggested a genetic localisation for the disease to chromosome 5q. Independent genetic linkage analysis in a six generation LCDI pedigree confirmed linkage to the 5q region bounded by marker loci IL9 and D5S436 suggesting genetic homogeneity. A maximum two point lod score of 7.51 (theta = 0.03) was obtained with marker D5S393. Multipoint and haplotype data positioned the disease between loci D5S393 and D5S396 corresponding to a genetic distance of 2cM, thus refining linkage sufficiently to allow for physical mapping of this disorder.

Chromosome Mapping↗
PubMed1995

Linkage refinement localises Sorsby fundus dystrophy between markers D22S275 and D22S278.

Sorsby fundus dystrophy is an autosomal dominant disorder which both clinically and histopathologically bears striking similarities to age related macular degeneration, one of the leading causes of blindness in the developed world. Recent studies have suggested a genetic localisation of the disease to chromosome 22q in a large genetic interval of approximately 25 cM. Independent genetic linkage analysis in a six generation British pedigree confirms linkage to the chromosome 22q region. A maximum two point lod score of 7.09 with no recombination was obtained with marker D22S280. Haplotype data positioned the disease between loci D22S275 and D22S278, thus significantly reducing the region on chromosome 22q where the gene is located.

Chromosomes, Human, Pair 22↗
PubMed1995

Seeding of YACs over regions 1q41-q42.3 and 11q14.3-q23 with microdissection clones.

We describe the use of pooled, region-specific hybridisation probes to screen high-density replica filters of a human genome YAC library. The probes were derived by microdissection of an approximately 30-Mbp region subtending the translocation breakpoint on a der(1)(1;11)(q42.1;q14.3) chromosome. Of 70 microdissection clones used in pools of 4-10, 47 identified a total of 77 YAC recombinants, representing over 50% of the microdissected region. This strategy can easily be adapted to other poorly mapped subchromosomal regions of the human or other mammalian genomes and will provide a solid framework for detailed contig map constructions.

Chromosomes, Artificial, Yeast↗
PubMed1995

Effect of storage at 4 degrees C and -20 degrees C on lipid, lipoprotein, and apolipoprotein concentrations.

We have investigated the effects on lipid, apolipoprotein, and lipoprotein measurements of storing unfractionated serum at 4 degrees C for 10 days and at -20 degrees C for 10 days or 3 months. Total serum concentrations of lipids were stable, although apolipoprotein B showed a 5.3% increase after 3 months at -20 degrees C (P < 0.001). Increases in low-density (LDL) and high-density lipoprotein (HDL) triglyceride and very-low-density lipoprotein (VLDL) esterified cholesterol concentrations and decreases in free cholesterol concentrations in LDL and HDL after storage of serum for 10 days at 4 degrees C were verified by fractionation of lipoproteins by sequential flotation ultracentrifugation. Ten days' storage of serum at -20 degrees C resulted in increases in VLDL triglyceride and phospholipid concentrations, with decreases in HDL concentrations in triglycerides and phospholipids; changes were more extensive after 3 months at -20 degrees C. We conclude that ultracentrifugation of serum for lipoprotein analysis should be performed as soon as possible after collection.

Apolipoproteins↗
PubMed1994

Simvastatin in non-insulin-dependent diabetes mellitus: effect on serum lipids, lipoproteins and haemostatic measures.

The clinical efficacy of the 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMGCoA) reductase inhibitor simvastatin in the treatment of hypercholesterolaemia in non-insulin-dependent diabetes (NIDDM), was examined in a double-blind placebo-controlled study of 6 months in 70 patients with NIDDM (age 25-70 years), of whom 57 were randomised to placebo (29 patients) or simvastatin for 6 months, following a 3-month run-in on diet. Patients were hypercholesterolaemic (7.8 (7.6-8.0) (mean (95% confidence intervals)) mmol/l simvastatin vs. 8.0 (7.7-8.5) mmol/l placebo) and mildly hypertriglyceridaemic (2.6 (2.2-3.0) simvastatin vs. 2.9 (2.3-3.5) placebo). Other lipid measures and estimates of glycaemic control and haemostasis were similar in both groups. There were no significant changes in lipids, haemostatic factors, or measures of glycaemic control in the placebo treatment group. Conversely by the end of 24 weeks, simvastatin produced a 28% reduction in cholesterol (to 5.6 (5.0-6.2) mmol/l (P < 0.001)), a 38% reduction in LDL cholesterol (from 5.5 (5.4-5.6) mmol/l to 3.4 (2.8-4.0) mmol/l, P < 0.001), a 15% reduction in triglyceride (to 2.2 (1.8-2.6) mmol/l, P < 0.05, and a 9% rise in HDL (from 1.16 (1.07-1.25) to 1.23 (1.14-1.32) mmol/l, P < 0.05). Improvements in apolipoprotein B (apo B) (-28%, P < 0.001), the LDL cholesterol to apo B ratio (-20%, P < 0.001), and apo A1 (+15%, P < 0.001) were recorded. There were no effects upon fibrinogen, factor VII activity, factor VIII activity, or measures of glycaemic control (fasting glucose, insulin, C-peptide, or HbA1).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Genetic linkage of cone-rod retinal dystrophy to chromosome 19q and evidence for segregation distortion.

Inherited retinal dystrophies are the most common cause of childhood blindness in the developed world. Cone-rod retinal dystrophies are severe examples of this group of disorders. Analysis of a large cone-rod dystrophy pedigree suggested that inheritance within the family was influenced by meiotic drive (p = 0.008), a rare segregation distortion in human genetics. Two-point linkage analysis showed significant linkage with three markers mapping to chromosome 19q. Multipoint analysis gave a maximum lod score of 10.08 (theta = 0.05) distal to D19S47. Cone-rod dystrophy is therefore assigned to 19q13.1-q13.2 and a new candidate locus for other retinal dystrophies is identified.

Child↗
PubMed1994

Identification of a sixth locus for autosomal dominant retinitis pigmentosa on chromosome 19.

We report the mapping of a sixth locus for autosomal dominant retinitis pigmentosa (adRP) to 19q13.4. After a total genome linkage search using over 300 markers in a single large pedigree, marker loci on the long arm of chromosome 19 showed significant linkage with the disease locus. Since the mapping information for the marker loci used in this study was derived from two different genome maps, we established genetic distances between relevant marker loci so that linkage information could be combined from both maps. A conventional three point analysis between the adRP phenotype and markers D19S180 and D19S214 gave a maximum lod score of 4.87. Combining data from these and other markers, we used the recently described multiple two point programme FASTMAP to simulate a multipoint analysis of the full data set. This gave a lod score of 5.34 in the interval between markers D19S180 and D19S214. Recently this laboratory has also reported the linkage of another form of retinal degeneration known as cone-rod dystrophy (CRD) to a genetically different set of markers from 19q. Linkage data presented here clearly supports the existence of two separate retinal genes in this part of the genome.

Chromosome Mapping↗